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Endocrinology > Exam 2 master file > Flashcards

Exam 2 master file Flashcards

1
Q

extracellular concentration of calcium

A

Total 2.5 x 10’-3 M; Free 1.2 x 10’-3 M

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2
Q

extracellular concentration of phosphate

A

Total 1.00 x 10’-3M;Free 0.85 x 10’-3 M

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3
Q

extracellular function of calcium ion

A

bone mineral; blood coagulation; membrane excitability

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4
Q

extracellular function of phosphate

A

bone mineral

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5
Q

how might anticoagulants work

A

against calcium ion

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6
Q

how does calcium ion affect membrane excitability

A

calcium channels, binding proteins, depolarization

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7
Q

intracellular calcium concentration

A

very low 10’-7 M

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8
Q

intracellular phosphate concentration

A

1.2 x 10’-3 M

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9
Q

intracellular calcium ion function

A

neuronal activation; hormone secretion; muscle contraction in all muscle types

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10
Q

why is intracellular calcium kept low

A

calcium can activate neurons and cause unwanted muscle contractions if unchecked

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11
Q

what is intracellular phosphate role

A

buffering; structure role; higher energy bonds (GTP, ATP); regulation of proteins by phosphorylation

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12
Q

where is 99% of calcium ion

A

in bone

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13
Q

how is calcium ion found in blood

A

50% is blood bound to albumin and globulins

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14
Q

what major hormones regulate Ca2+

A

PTH, vitamin D, and calcitonin

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15
Q

Where is calcium from

A

diet; GI tract is major source;

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16
Q

how does calcium travel from GI tract

A

half excreted; half absorbed in blood; 10 mmol travel back and forth between blood and bone; 240 mmol are sent from blood to kidney; 233 mmol go back to blood

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17
Q

what is grab and release

A

what bone does with calcium from blood; sends it back; in adults it is balanced because there is no bone growth

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18
Q

major glands in charge of calcium regulation

A

thyroid and parathyroid

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19
Q

cells in thyroid gland

A

follicular and parafollicular cells

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20
Q

what is important about parafollicular cells

A

involved in secreting calcitonin; AKA “C-cells”

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21
Q

how does parathyroid present

A

at least four of these glands in one person. Tiny, from 30-50 mg. Sometimes parathyroid sits with thymus, which happens during embryogenesis.

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22
Q

what is calcitonin

A

a peptide

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23
Q

what do calcitonin and PTH have in common

A

a precursor. But then it is cleaved. PTH precursor is made in thyroid. Calcitonin precursor is made in brain.

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24
Q

CGRP

A

calcitonin gene related peptide

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25
Q

cells of parathyroid

A

chief cells and oxyphil cells

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26
Q

what do chief cells secrete

A

PTH

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27
Q

what is parathyroid related hormone (PTHrP)

A

a hormone that is a precursor to PTH, related, but PTH is cleaved from PTHrP

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28
Q

how does serum calcium affect PTH

A

if calcium goes up, PTH goes down and vice versa. Inverse relationship.

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29
Q

what is calcium sensor

A

7TM domain

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30
Q

7TM domain

A

large; changes conformation on the basis of calcium levels in serum

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31
Q

what does calcium activate if there are high levels of it

A

phospholipase. Inhibits PTH secretion and synthesis.

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32
Q

what does calcium activate if there are low levels of it

A

adenylate cyclase cyles. Increases PTH secretion and synthesis.

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33
Q

How is either calcium pathway chosen

A

chosen by sensor and G protein has to be chosen that will activate each specific pathway.

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34
Q

PTH receptor

A

G protein linked

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35
Q

what binds to PTH receptor

A

both PTH and PTHrP

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36
Q

How does PTH regulate calcium

A

PTH activates adenylate cyclase, which activates cAMP production in kidney, which causes retention of Ca in distal convoluted tubule and inhibition of phosphate reabsorption in proximal tubule. Clinically, see more cAMP and phosphate in urine.

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37
Q

what is source of vitamin D, besides sunlight

A

diet

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38
Q

what is vitamin D

A

a classical steroid hormone

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39
Q

transcalciferin

A

Vitamin D transporter

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40
Q

good source of vitamin D

A

fish, because they consume plankton

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41
Q

why do we need to consume vitamin D in an oil

A

it is hydrophobic. Will go right through consumer if taken with water.

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42
Q

what is VDRE

A

vitamin D response element

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43
Q

where is VDRE

A

in promoter domain. Receptor binds to the sequences on VDRE, right?

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44
Q

How does PTHR activate adenylate cyclase

A

Gs activates AC

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45
Q

how deos PTHR activate phospholipase

A

Gq

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46
Q

target tissue of vitamin D

A

Gi tract, bone and kidney

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47
Q

effects of vitamin D

A

uptake of calcium in GI tract because vitamin D increases production of calbindin via gene transcription

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48
Q

calbindin

A

protein that binds to calcium in cytoplasm

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49
Q

what are the two calcium pathways in GI tract

A

active and passive

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50
Q

active pathway for calcium in GI tract

A

specialized transporter with pumps pumps calcium into cell. Calcium binds to calbindin, which shuttles it to other side of cell and pushes it out of cell.

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51
Q

passive pathway for calcium in GI tract

A

calcium travels between cells. Works well when there are large amounts of calcium consumed.

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52
Q

why might it be good to upregulate active transport of calcium

A

to prevent osteoporosis

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53
Q

how does calcium travel in kidney

A

similar pathway to GI tract. Reuptake in distal tubule and upregulation of calcium binding protein.

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54
Q

what is the calcium depot in the body

A

bone(storage and relase system)

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55
Q

what cells make up bone

A

osteoblasts, osteocytes, and osteoclasts

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56
Q

osteoblast function

A

secrete osteoid to form bone, calcify, help with remodeling

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57
Q

osteocyte function

A

made from osteoblasts; hardened in mineral; responsible for blood maintenance like toxin removal and nutrient uptake

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58
Q

osteoclast function

A

responsible for bone degradation

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59
Q

mesenchymal cells

A

differentiate and form osteoblasts

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60
Q

how do osteoblasts become osteocytes

A

osteoblasts become trapped in matrix and cant divide

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61
Q

how do osteoclasts raise blood calcium levels

A

they digest bone and release calcium from bone

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62
Q

what receptors are on osteoblasts

A

alkaline phospholypase, PTHR, IGF-1R

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63
Q

what do osteoblasts produce

A

Type 1 collagen and various noncollagenous proteins

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64
Q

what are noncollagenous proteins

A

osteocalcin, osteonectin, osteopontin, bone sialoprotein, osteoprotegerin, macrophage-colony, stimulating factor

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65
Q

osteocalcin

A

regulated by Vitamin D; has high binding affinity to hydroxyapatite Ca5(PO4)3(OH)

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66
Q

how do osteocytes work

A

sit in bone; interact by projections; close to blood vessels; excrete toxins/take up nutrients from blood

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67
Q

where are osteoclasts located

A

in concave ares called resorption cavities or Howship’s Lacunae

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68
Q

what does osteoclast secrete

A

protons and lysosomal enzymes that mediate osteolysis

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69
Q

what do calcitonin receptors do on osteoclasts

A

they inhibit degradation of bone

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70
Q

Vitamin D formation cycle

A

start with a cholesterol – 7-dehydrocholesterol/ irradiate with UV light (skin) → one of the rings breaks –> chelecalciferol (vitamin D3) –> suffers 25-hydroxylation in liver –> becomes 25 hydroxychotecalciferol (25-COH)D3 → treated with either 1. hydroxylation or 24. hydroxylation in kidney → becomes 1,25-dyhydroxycholescalciferol or 24,25-dihydroxycholescalciferol

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71
Q

mechanism of vitamin D in target cells

A

enters nucleus → in nucleus is VDRE, TATA and ATG → at VDRE is bound heterodimer RXR/VDR (coinhibitors are available) → D binds to its receptor on VDRE → string of coactivators complex binds to D and connects it to RNA polymerase II on TATA box(initiation complex)→ transcribes mRNA –> ATG is methionine start codon, which waits in nucleus

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72
Q

how do osteoclasts form? What is their function?

A

fusion of macrophages to form large multinucleated cells. They break down bone matrix.

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73
Q

where do osteoblasts come from?

A

from mesenchymal cells. Make protein matrix -osteoid and calcification hydroxyapatite

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74
Q

how do osteocytes form

A

osteoblasts trapped in matrix. Concerned with bone maintenance.

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75
Q

what parts of osteocytes do the work

A

canaliculi and gap junctions

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76
Q

howship’s lacunae

A

invaginations in bone to which osteoclasts attach and release enzymes and H+ and Cl-

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77
Q

what does calcitonin do to bone

A

it has receptors on osteoclasts and inhibits secretory and digestive properties of osteoclasts

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78
Q

how do osteoclasts work

A

form ruffled border between itself and invagination; pump in Cl- and H+; makes more acidic; lysosomal enzymes

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79
Q

how does PTH elevate calcium levels in blood

A

recruits precursors of macrophages that become osteoclasts; indirectly activates osteoclasts by stimulating osteoblasts; upregulates M-CSF and down regulates osteoprotegerin

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80
Q

what does osteoprotegerin do

A

it blocks RANKL from binding with its receptor on macrophage that will become osteoclast

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81
Q

how does M-CSF work

A

binds with macrophage that becomes osteoclast

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82
Q

steps of osteoclast differentiation

A

first, monocyte; second, becomes macrophage and binds M-CSF, which makes it express RANK receptor; third, binds RANKL and is bound to osteoblast; fourth; disassociates from osteoblast but is inactive; fifth, becomes inactive when ruffle forms and and sealing zone form

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83
Q

what is alpha v beta 3 integrin

A

binds to osteoclasts to form sealing zone

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84
Q

How does vitamin D affect calcium ion?

A

Vitamin D increases Ca; it increases Ca ion transport in intestine and kidney by upregulating transcription and translation of calcium binding protein; 2. regulates osteoclast activity in the bone

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85
Q

How does PTH regulate calcium

A
  1. increases retention of calcium by kidney and decreases retention of phosphate 2. increases production of calcitriol (active Vitamin D) by kidney 3. osteoclast upregulation, albeit indirectly
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86
Q

how does calcitonin work

A

calcitonin decreases Ca 1. direct inhibition of osteoclast activity in bone 2. increased loss of calcium and phosphate in the kidney filtrate

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87
Q

how does prostaglandin E2 affect calcium

A

increases osteoclast activity

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88
Q

what does mechanical stress do

A

signals need for bone remodeling

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89
Q

what does thyroid do to calcium

A

stimulates osteoclast activity

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90
Q

how does bone immobilization affect calcium homeostasis

A

it increases bone resorption and decreases bone formation ; it increases serum Ca, which decreases PTH. Both increase urine Ca. Decrease in PTH causes decrease Vitamin D, which causes decrease in intestinal calcium absorption

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91
Q

how does exercise affect calcium homeostasis

A

it decreases bone resorption and increases bone formation; it decreases serum Ca, which increases PTH; both lead to decrease in urine Ca. Increase in PTH causes increase in vitamin D; which causes increase in intestinal Ca absorption

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92
Q

growth hormone and calcium

A

mechanism: signals somatomedin C (IGF-1) release from liver; effect: increases bone and cartilage growth

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93
Q

thyroid hormones and ca

A

mechanism: secretions from thyroid gland follicular cell; increases bone and cartilage growth

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94
Q

PTH

A

low blood ca signals relase from parathyroid gland; PTH signals osteoblasts to stimulate osteoclast activity; stimulates osteoclast line development from CFU-GM and bone resporptive activity; inhibits alkaline phosphatase of osteoblast

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95
Q

calcitonin

A

high blood ca signals thyroid c-cell to secrete it; directly inhibits osteoclasts

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96
Q

sex hormones

A

estradiol and testosterone affect cartilage and bone growth; complex actions: stimulate bone growth; leads to closing of growth plate; too much; dwarfism, too little: gigantism, osteoporosis

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97
Q

vitamin A

A

binds to receptors on osteoclasts and releases proteases from chondrocytes; signals bone resorption; signals cartilage resorption

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98
Q

vitamin C

A

cofactor for proline hydroxylase in collagen synthesis; supports collagen formation

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99
Q

vitamin D

A

stimulates ca uptake from gut; stimulates production of osteonectin by osteoblast; stimulates osteoclast development from CFU-MG stem cell; supports mineralization of bone and cartilage; stimulates bone turnover

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100
Q

bone growth promoters

A

insulin, somatomedins, vitamin K

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101
Q

bone grrowth inhibitors

A

sglucocorticoids

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102
Q

how do PTH, vitamin D and FGF23 interact

A

PTH to kidney; upregulate vitamin D; Vitamin D to PT gland; down regualte PTH; vitamin D to bone; upregulate FGF23; bone to kidney, down regulate vitamin D

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103
Q

integrated response to hypocalcemia

A

four responses: calcium sensor taks to PT gland; increase PTH; increase D; increase gut absorption; calcium sensor talks to thyroid c-cells – decrease calcitonin – increase bone resorption (PTH does this as well); ca sensor talks to kidney – increase renal ca absorption (PTH) and decrease urinary ca excretion; renal ca filtration decreases, which decreases ca in urine

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104
Q

integrated response to hypercalcemia

A

foru responses: calcium sensor talks to PT gland – down PTH – down D-down gut absorption; sensor talks to c-cells – up calcitonin – down bown resporption (PTH as well causes this); sensor talks to kidney – down renal ca reabsorption – increase ca in urine – up renal ca filtration, which increases ca urine

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105
Q

how does vitamin D affect bone, kidney, gut, blood calcium

A

bone: up o/c activity, up bone resorption; kidney: up ca reabsorption, up phosphate reabsorption; gut: up calcium absorption, up phosphate absorption; blood: up calcium and phosphate

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106
Q

how does PTH affect bone, kidney, gut, blood calcium

A

bone: down o/b activity, up bone resorption; kidney – up 1alpha hydroxylase synthesis, up ca reabsorption, down phosphate reabsorption; gut – up ca absorption, up phosphate absorption by indirect action only; blood – up ca and down phosphate

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107
Q

how does calcitonin affect bone, kidney, gut, blood calcium

A

bone: down o/c activity, down bone res.; kidney – down ca reab, down p reab; gut – nothing; blood – down ca and p

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108
Q

symptoms of hypocalcemia 4

A

muscle cramps, numbness, parasthesia, mood swings and depression

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109
Q

signs of hypoclacemia 5

A

tetany, carpopedal spasm, neuromuscular activity, convulsions, cardiac arrhythmias, cataract

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110
Q

symptoms of hypercalcemia 8

A

bony pain, abdominal pain from peptic ulceration, acute pancreatitis or constipation, anorexia and nausea, thirst and polyuria, muscle weakness, headache and confusion, palpitations through cardiac arrhythmias, tiredness and fatigue

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111
Q

signs of hypercalcemia 5

A

renal stones, bone fractures, convulsions and coma if severe, corneal calcification, hypertension

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112
Q

what can cause bone changes by hyperparathyroidism

A

many tumors secrete PTH or PTHrP and thus cause generalized demineralization as seen in phalanges of the hand

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113
Q

rickets and osteomalacia

A

disorders of mineralization of organic matrix (D deficiency)

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114
Q

osteoporosis

A

metabolic bone disease with decreased bone mass

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115
Q

paget’s disease

A

uncontrolled, large osteoclasts cause bone demineralization

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116
Q

osteopetrosis

A

high density bone with occlusion of marrow spaces and subsequent anemia due to lack of osteoclastic activity

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117
Q

jensen’s disease or metaphysial chondrodysplesia

A

causes dwarfism due to deficiency in PTH or PTHrP or its respective receptors

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118
Q

symptoms of vitamin D deficiency

A

pains and aches; severe pain, weakness; osteomalacia; bone pains (hips, ribs, feet, pelvis and thighs)

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119
Q

adult vitamin d deficiency symptoms

A

poor immune system, osteoporosis, mood changes, heart problems and high BP, chronic diseases like crohn’s disease and MS, dental problems like gum disease, asthma, bone disease development called osteomalacia

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120
Q

How is energy stored in body?

A

as glycogen and fat

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121
Q

how often does fuel metabolism change

A

several times a day, between catabolic and anabolic phases

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122
Q

how are higher brain centers stimulated to influence the gut

A

taste, smell, sight, thought, etc.

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123
Q

What does higher brain send signals to

A

hypothalamus

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124
Q

what does hypothalamus send signals to?

A

it sends signals back to higher brain and it sends hunger or satiety signals to the gut

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125
Q

what signals does the gut send?

A

the gut stimulates the vagus (SNS) catabolic process and releases CCK in the short term. In the long term, the gut releases hormones that are substrates to the pancreas, which in turn produce insulin, which helps build WAT, and which releases leptin, which also stimulates the SNS anabolic pathway

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126
Q

what signals does the SNS send?

A

it signals the pancreas to produce insulin, which help add WAT and leptin. It also stimulates BAT and heat production.

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127
Q

catabolism

A

tears down molecules

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128
Q

anabolism

A

builds up molecules

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129
Q

what makes up the oral cavity? What is it responsible for?

A

mouth and pharynx, salivary glands; chewing begins, initiation of swallowing

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130
Q

what are the exocrine secretions of the salivary glands

A

salt and water – moisten food; mucus – lubrication; amylase – polysaccharide-digesting enzyme

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131
Q

what is role of esophagus

A

moves food to stomach by peristaltic waves

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132
Q

what are esophagus exocrine secretions

A

mucus for lubrication

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133
Q

role of stomach

A

store, mix, dissolve and continue digestion of food; regulates emptying of dissolved food into small intestine

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134
Q

exocrine secretions of stomach

A

HCL – solubilization of food particles, kill microbes, activation of pepsinogens to pepsins; Pepsins – protein-digesting enzyme; mucus – lubricate and protect epithelial surface

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135
Q

role of pancreas

A

secretion of enzymes and bicarbonate; also has nondigestive endocrine functions

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136
Q

exocrine secretions of pancreas

A

Enzymes – digest carbs, fats, proteins and nucleic acids; bicarbonate – neutralize HCL entering small intestine from stomach

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137
Q

liver role

A

secretion of bile; many other nondigestive functions

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138
Q

exocrine secretions of liver

A

bile salts – solubilize water – insoluble fats; bicarb – neutralize HCL entering small intestine from stomach

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139
Q

role of gallbladder

A

store and concentrate bile between meals

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140
Q

role of small intestine

A

digestion and absorption of most substances, mixing and propulsion of contents

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141
Q

exocrine secretions of small intestine

A

Enzymes – food digestion; salt and water – maintain fluidity of luminal contents; mucus - lubricataion

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142
Q

role of large intestine

A

storage and concentration of undigested matter; absorption of salt and water; mixing and propulsion of contents; defecation

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143
Q

exocrine secretions of large intestine

A

lubrication

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144
Q

anatomical features of gut in order from inside to out

A

lumen, mucosa, submucosa, submucosal nerve plexus, circular muscle, myenteric plexus, longitudinal muscle, serosa. There is sympathetic and parasympathetic input to gut

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145
Q

will myenteric plexus move on its own

A

it is autonomic; will contract without attachment to body. It is a network of mesh.

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146
Q

how do enteroendocrine cells present in gut

A

they are present in most of GI tract distributed as single cells throughout gastrointestinal epithelium

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147
Q

largest endocrine “organ”

A

enteroendocrine cells

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148
Q

does enteroendocrine cell reach epithelial surface

A

no

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149
Q

what are the two types of enteroendrocrine cells

A

lingual taste-receptor cell and intestinal enteroendocrine cell

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150
Q

what is ligand that signals enteroendocrine cells

A

food

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151
Q

How does a lingual taste receptor cell work

A

G protein activates phospholipase Cbeta2; which makes IP3, which increases Ca2+ in cytoplasm, which causes release of neurotransmitters that stimulate afferent nerve

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152
Q

what three channels exist on lingual taste receptor

A

Sodium /transient receptor potential channels’ de;ayed-rectifying K+ channels; calcium voltage gated channels

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153
Q

how does intestinal enteroendocrine cell work

A

via nutrient ligand, binds to receptor, activates Galpha protein that activates phospholipase, which synthesizes IP3, increases intracellular calcium, and secretes GLP1 into bloodstream and vagal or spinal nerve

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154
Q

what channels live on intestinal enteroendocrine cell

A

sodium/TRPMS

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155
Q

model to increase ghrelin secretion

A

bitter tastants bind to taste receptors on ghrelin cell or on the brush cells in the GI tract, and couple via alpha-gustducin to increase ghrelin secretion

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156
Q

what does increased ghrelin secretion result in

A

short term increase in food intake and accelerated grastric emptying; followed by a prolonged decrease in food intake

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157
Q

what does decrease in food intake correlate with

A

delay in grastric emptying

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158
Q

what does alpha-gustducin do?

A

it is involved in sensing the medium chain fatty acid (MCFA) octanoic acid in the diet

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159
Q

what is octanoic acid necessary for in diet

A

the octanoylation of ghrelin

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160
Q

what receptor may play a role in the lipid sensing cascase in ghrelin-producing cells

A

GPR120

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161
Q

what two hormones are produced in the pyloric antrum?

A

gastrin and glucagon

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162
Q

gastrin function

A

stimulates release of HCL and pepsinogen

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163
Q

glucogen function

A

promotes conversion of glycogen to glucose in the liver

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164
Q

what four hormones are produced in the duodenum and jejunum?

A

cck, gastric inhibitory peptide, motilin, and secretin

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165
Q

cholecystokinin

A

stimulates pancreatic enzyme release and elicits gallbladder contraction

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166
Q

gastric inhibitory peptide

A

stimulates insulin secretion

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167
Q

motilin

A

stimulates gastrointestinal motility

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168
Q

secretin

A

stimulates bicarbonate and water secretion by pancreatic duct cells

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169
Q

what hormone does the ileum produce?

A

neurotensin

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170
Q

neurotensin

A

inhibits GI motility

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171
Q

what hormone does large intestine make?

A

glicentin

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172
Q

glicentin

A

promotes conversion of glycogen to glucose in liver

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173
Q

what hormones are produced in stomach, small intestine and large intestine?

A

somatosatin, serotonin, substance P

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174
Q

somatostatin

A

inhibits local secretion of gastrin, motilin, secretin, and gastric inhibitory peptide + other actions

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175
Q

serotonin

A

stimulates gastrointestinal motility

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176
Q

substance P

A

stimulates intestinal motility

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177
Q

where is gastrin released in large intestine? By when does it diminish?

A

antrum/ ileum

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178
Q

order of large intestine parts

A

fundus, antrum, duodenum, jejunum, ileum, colon

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179
Q

where is CCK release in large intestine? By where does it diminish?

A

duodenum/colon

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180
Q

where is secretin released in large intestine? By where does diminish?

A

duodenum/colon

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181
Q

where is GIP secreted in large intestine? By where does it diminish?

A

duodenum/ileum

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182
Q

Are VIP, Motilin or somatostatin secreted in large intestine?

A

no, but they are present still

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183
Q

what stimuli in cephalic phase control HCL secretion during a meal? What pathway is used?

A

sight, smell, taste, chewing ; parasympathetic nerves to ENS

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184
Q

what stimuli in gastric phase control HCL secretion during a meal? What pathway is used?

A

distension, increase in peptides, decrease in proton concentration; long and short neural reflexes and direct stimulation of gastrin secretion

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185
Q

what stimuli in intestinal phase control HCL secretion during a meal? What pathway is used?

A

distension, increase in proton concentration, increase in osmolarity, increase in nutrient concentrations; long and short neural reflexes; secretin, CCK, and other duodenal hormones

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186
Q

three phases of digestion

A

cephalic, gastric and intestinal

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187
Q

what sphincter is next to esophagus at entrance to stomach

A

cardiac sphincter

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188
Q

what sphincter is at end of stomach

A

pyloric sphincter

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189
Q

layers of stomach wall from luminal to basolateral

A

glands that secreted gastric juice, gastric glands, circular muscle, longitudinal muscle

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190
Q

through what is gastric released into lumen

A

the gastric fundic region

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191
Q

what makes up gastric fundic region, from luminal to basolateral

A

pit, isthmus, neck, and base

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192
Q

what cells line the gastric fundic region?

A

mucous neck cells (in neck), parietal cells, enteroendocrine cells, chief (zymogenic cells)

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193
Q

what are the two secretory cells of the stomach

A

chief cell and parietal cell

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194
Q

what makes up inside of chief cell?

A

zymogen granules, and extensive rER

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195
Q

what makes up inside of parietal cell?

A

tobulovesicular system, intracellular calaliculus, few ribosomes and lysosomes

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196
Q

what does chief cell produce?

A

precursor enzyme of the gastric secretion; pepsinogen and lipase

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197
Q

what does parietal cell produce?

A

HCL and intrinsic factor for vitamin B12

198
Q

what is at luminal side of both chief and parietal cells

A

junctional complexes

199
Q

what three receptors does parietal cell have?

A

histamine H2, acetylcholine, and gastrin

200
Q

what secretes gastrin? How does it get to parietal cell?

A

G cell. Through the bloodstream.

201
Q

what secretes histamine?

A

ECL cell

202
Q

What stimulates G cell to secrete gastrin?

A

vagus nerve stimulates post synaptic neuron, which releases gastrin releasing peptide

203
Q

what stimulates ECL cell to release histamine?

A

postganglionic cholinergic nerve releases neurotransmitters that bind with receptor on ECL cell

204
Q

what secretes acetylcholine?

A

a neuron

205
Q

What hormones regulate the parietal cell?

A

gastrin, histamine, acetylcholine, somatostatin, gastrin releasing peptide

206
Q

how is acetylcholine a major secretagogue?

A

it stimulates secretion of pepsinogen by chief cells of stomach

207
Q

is gastrin an important secretagogue

A

it is only effective in vitro and at high concentration

208
Q

what kind of secretory cells do pancreas have?

A

exocrine and endocrine

209
Q

which pancreatic cells secrete enzymes?

A

exocrine cells

210
Q

which pancreatic cells secrete bicarbonate?

A

duct cells

211
Q

what runs along length of pancreas

A

pancreatic duct

212
Q

what role do pancreas play

A

main digestive gland in our body

213
Q

what enzymes do the pancreas secrete?

A

trypsin, chymotrypsin, steapsin, carboxypeptidase, elastases, nucleases, and pancreatic amylase

214
Q

trypsin

A

protease that cleaves proteins at the basic amino acids

215
Q

chymotrypsin

A

protease that cleaves proteins at the aromatic amino acids

216
Q

steapsin

A

degrades triglycerides into fatty acids and glycerol

217
Q

carboxypeptidase

A

protease that takes off the terminal acid group from a protein

218
Q

elastase

A

degrades the protein elastin and some other proteins

219
Q

nucleases

A

degrade nucleic acids, like DNAase and RNAase

220
Q

pancreatic amylase

A

degrades starch, glycogen and most other carbohydrates

221
Q

bicarb regulation cycle

A

increase in acid from stomach; increase in secretin secretion in small intestine; increase in plasma secretin; the Panceas increase bicarb secretion, which increases flow of bicarb into small intestine, which neutralizes the intestinal acid put there by stomach. Once pH goes up, this provides negative feedback to small intestine’s secretin secretion.

222
Q

fatty acid and amino acid digestion cycle between SI and pancreas

A

increase in intestinal fatty acids and amino acids; increase in CCK secretion in small intestine; increase in plasma CCK; stimulates pancreas to increase enzyme secretion; increases flow of enzymes into small intestine, which leads to increase in digestion of fats and proteins in SI

223
Q

what part of SI is ileum?

A

Last part before colon

224
Q

portal vein flows from small intestine to?

A

liver

225
Q

bile flows from and to?

A

liver and gallbladder to small intestine

226
Q

what are six main ingredients of bile?

A

bile salts; lecithin; bicarb ions and other salts; cholesterol; bile pigments and small amounts of other metabolic end-products; protein (IgA) and peptides, and trace metals

227
Q

how do gallstones form?

A

when concentration of cholesterol in the bile becomes high in relation ot the concentrations of phospholipids and bile salts, cholesterol crystallizes out of solution and causes gallstones

228
Q

enterohepatic circulation of bile salts

A

bile salts are secreted into bile and enter the duodenum through the common bile duct. Bile salts are reabsorbed from the intestinal lumen into hepatic protal blood. The liver reclaims bile salts from hepatic portal blood.

229
Q

what is preprograstrin

A

precursor to gastrin

230
Q

what do the structures of gastrin and cck both contain

A

sulfated tyrosine residue

231
Q

which adiposity signals work straight with hypothalamus (3)

A

adiponectin, insulin, and leptin

232
Q

Which gut hormones act directly with hypothalamus (3)

A

PYY, OXM, Ghrelin

233
Q

Which gut hormones act directly with brainstem?

A

PP, GLP-1, CCK

234
Q

which gut hormones and adipose signals influence vagus?

A

adiposity signals: leptin; gut: ghrelin, PP, GLP-1, and CCK

235
Q

what does antral mucosa secrete?

A

gastrin

236
Q

what do pancreas secrete?

A

insulin, glucagon, somatostatin, pancreatic polypeptide

237
Q

what does upper small intestine secrete?

A

secretin, CCK, GDIP, motilin

238
Q

what does lower small intestine secrete?

A

neurotensin, enteroglucagon

239
Q

what do pancreatic islets of langerhans secrete?

A

insulin, glucagon, and somatostatin

240
Q

what do pancreatic endocrine cells secrete?

A

pancreatic polypeptides

241
Q

role of CCK in digestion

A

slows down emptying of the stomach by acting on pyloric sphincter; stimulates bile release from the galbladder and the secretion of pancreatic enzymes

242
Q

role of secretin in digestion

A

stimulates pancreatic bicarb secretion; enhances insulin secretion by B cells of the islets of langerhans

243
Q

role of gastrin in digestion

A

stimulates HCL secretion in parietal cells; stimulates insulin secretion by B cells of islets of langerhans; stimulates gastric motility and growth of mucosal cell

244
Q

digestion

A

breaking proteins, fats and carbs into absorbable units (principally in small intestine)

245
Q

absorption

A

products of digestion and vitamins, minerals and water cross the mucosa and enter lymph or blood

246
Q

how do mixed amino acids reach the liver?

A

via the portal vein

247
Q

what are branched amino acids used for?

A

protein synthesis under influence of insulin

248
Q

how are amino acids and di and tripeptides absorbed?

A

across symporter channels together with Na+. The transport is active.

249
Q

where does protein digestion start?

A

in the stomach, in the presence of pepsin.

250
Q

what is pepsin derived from?

A

precursor pepsinogen secreted by chief cells

251
Q

where does pepsin activity end?

A

in alkaline environment of duodenum.

252
Q

what pancreatic proteases continue proteolysis?

A

endopeptidases and exopeptidases

253
Q

what activates trypsinogen? Where?

A

enterokinase turns trypsinogen to trypsin on the microvilli. Trypsin in turn activates the bulk of trypsinogen.

254
Q

what activates chymotrypsinogen and proelastase?

A

chymotrypsin and elastase, respectively

255
Q

what are carboxypepsidasea A and B derived from?

A

procarboxypeptidase A and B precursors

256
Q

in what does trypsin play a significant role?

A

it activates and inactivates pancreatic proenzymes.

257
Q

how are tripeptides in cytosol digested?

A

by cytoplasmic peptidases into amino acids

258
Q

what is daily protein requirement for adults?

A

0.8 g/kg body weight. Higher in pregnant women, postsurgical patients and athletes.

259
Q

why must nine essential amino acids be in diet?

A

because body cannot synthesize them.

260
Q

in what two ways does glucose from diet enter hepatic glycogen?

A

a. 50% glycogen formed from ingestd glucose directly, without degradation; remainder is converted to lactate in peripheral and splanchnic tissues

261
Q

how is glucose converted to lactate in peripheral and splanchnic tissues?

A

15-20% of glucose converted to lactate in subcutaneous adipose tissue and CNS and RBC; lactate returns to liver and is coverted to G-6-phosphate via gluconeogenesis; lactate also from intestinal metabolism of either circulating or newly absorbed glucose.

262
Q

what are the main dietary carbs?

A

starch, sucrose, lactose and maltose

263
Q

starch?

A

amylose and amylopectin

264
Q

sucrose?

A

glucose, fructose disaccharide

265
Q

lactose?

A

Galactose-glucose disaccharide

266
Q

maltose?

A

glucose dimer

267
Q

what initiates digestion of starch?

A

salivary alpha-amylase in the mouth

268
Q

what completes starch digestion?

A

pancreatic alpha-amylase in small intestine

269
Q

oligosaccharidases

A

(sucrase, lactase, isomaltase), hydrolyze major dietary sugars; present in PM of microvilli

270
Q

why is cellulose not digested by humans?

A

cellulase is not present. Cellulose accounts for undigested dietary fiber.

271
Q

what is bile salt?

A

glycocholic acid

272
Q

what is fat emulsified by?

A

bile salts and phospholipids

273
Q

what is emulsification?

A

fat globule and bile salt and phospholipid

274
Q

what do fat droplets become with bile salt and phospholipids?

A

emulsion droplets

275
Q

add bile salts and pancreatic lipase to emulsion droplets and get?

A

micelles

276
Q

what happens to emulsion micelles once they are formed?

A

they become free molecules of fatty acids and monoglycerides that can diffuse through lipid bilayer. They are treated by triglyceride synthetic enzymes in endoplasmic reticulum and become chylomicrons

277
Q

chylomicron

A

droplets of triglyceride enclosed by membrane from the endoplasmic reticulum

278
Q

where are lipids stored?

A

adipose tissue

279
Q

what is the purpose of adipose tissue?

A

adaptation to famine

280
Q

how do lipids travel in circulation?

A

dietary lipids cross through intestinal cell; become chylomicrons; enter capillaries; are treated by lipoprotein lipase; chylomicron remnants go to liver and are received by remnant receptors

281
Q

what induces the phosphorylation of lipase?

A

epi, glucagon and ACTH

282
Q

what does phosphorylation of lipase result in?

A

mobilization of triglyceride pool/ lypolytic effect

283
Q

what inhibits lipase activity?

A

insulin and prostaglandins

284
Q

what does lipase inhibition cause?

A

lipid storage, or antilypolytic effect

285
Q

two clinical conditions associated with adipose tissue

A

obesity and diabetes

286
Q

leptin is produced by?

A

white adipose tissue

287
Q

leptin provides what?

A

information about fat mass and nutritional status to neural centers regulating appetite, energy balance and feeding

288
Q

GLUT-4

A

glucose transporter protein; produced by adipocyte; facilitates entrance of glucose to the cell

289
Q

lipoprotein lipase synthesized by? Transferred to?

A

synthesized by adipose cell and transferred to endothelial cell

290
Q

catabolism: how does liver produce glucose?

A

via glycogen breakdown and via gluconeogenesis

291
Q

what is glucose preserved for?

A

CNS

292
Q

what do tissues besides CNS preferentially use for energy?

A

long chain fatty acids and their derivative products – ketone bodies

293
Q

what can brain also use, besides glucose

A

ketones

294
Q

what does lipolysis release?

A

glycerol

295
Q

where does pyruvate lactate come from?

A

muscle glycogen

296
Q

where do amino acids come from?

A

proteolysis

297
Q

what are three additional gluconeogenesis substrates?

A

glycerol, pyruvate/lactate, amino acids

298
Q

where do hunger and satiety originate?

A

from afferent neuronal and humoral signals from the GI tract, adipose tissue, and other peripheral organs to the brain

299
Q

from where do hypothalamus and brainstem receive signals to coordinate feeding and metabolic adaptations?

A

nutrients, GI hormones, adipokines, and vagal afferents

300
Q

when are peripheral stimuli and inhibitors to digestion released?

A

in anticipation or response to food

301
Q

what can peripheral stimuli and inhibitors cross?

A

blood brain barrier

302
Q

what is role of peripheral stimuli and inhibitors?

A

activate/release/synthesize central factors in the hypothalamus that either increase or decrease subsequent food intake

303
Q

where do executive functions originate?

A

frontal cortex

304
Q

central inhibitors (5)

A

POMC, CART, CCK, NE, CRH

305
Q

central stimuli (3)

A

NYY, orexin-A, cannabinoids

306
Q

when stomach releases ghrelin and cortisol, what do they stimulate?

A

they cross the BBB and stimulate NYY, orexin-A and cannabinoids

307
Q

list peripheral inhibitors (7)

A

glucose/AA/FFA, CCK, PYY, insulin, leptin

308
Q

how is ghrelin initially synthesized?

A

as a preprohormone

309
Q

how is ghrelin processed?

A

proteolytically processed to yield 28 aa peptide

310
Q

when is ghrelin produced and secreted?

A

by stomach as early response to food

311
Q

in the brain, what is source of ghrelin?

A

hypothalamus

312
Q

where else, other than hypothalamus and stomach, is ghrelin made?

A

placenta, kidney and pituitary gland

313
Q

What 3 major regions of brain does ghrelin stimulate?

A

hindbrain, hypothalamus, mesolimbic reward system in midbrain

314
Q

role of hindbrain

A

controls automatic processes

315
Q

role of hypothalamus

A

regulates metabolism

316
Q

when does ghrelin spike?

A

before routine meal times.

317
Q

when does ghrelin spike for grazing animals?

A

they have little spikes all day

318
Q

from what are glucagon, oxyntomodulin, NPGF and glicentin derived?

A

from a larger, common precursor that has 158 aa

319
Q

what does oxyntomodulin do?

A

it acts to suppress appetite

320
Q

what were results of parabiosis study of Ob/Ob and Db/Db mice?

A

Ob and WT – slimmer OB, normal WT; Db and WT – normal Db and slimmer WT; Ob and Db – slimmer Ob and normal Db.

321
Q

how big is leptin?

A

16 Kda protein hormone

322
Q

where is leptin made?

A

synthesized and secreted by adipose tissue and the placenta

323
Q

of what gene is leptin a product?

A

Ob gene, on chromosome 7q31.3-32

324
Q

what is main target of leptin?

A

hypothalamus

325
Q

what kind of receptor does leptin have?

A

cytokine receptor group of cell surface receptors

326
Q

what is intracellular signaling apparatus of leptin receptor?

A

JAK-STAT

327
Q

leptin binding protein

A

soluble isoform of ectodomain of leptin receptor forms a binding protein in circulation

328
Q

main actions of leptin

A

suppress appetite; increases energy expenditure

329
Q

leptin and fasting

A

plasma leptin is very low, so stored energy is conserved

330
Q

nonfasting and leptin

A

circulating leptin increases with adiposity

331
Q

rhythm of circulating leptin

A

exhibits circadian rhythm; highest around midnight with nadir around middday

332
Q

relative levels of plasma leptin throughout life in newborn, childhood, puberty and adulthood?

A

Newborn – high; childhood – low; puberty – leptin increases early in puberty. In boys, increase is only transient. In girls, sustained. ; adulthood – leptin higher in women than men

333
Q

how do environment and lifestyle influence food intake and energy expenditure in brain?

A

cognition; reward; choice; mood; stress

334
Q

how does brain respond to environmental stimuli?

A

energy intake or expenditure

335
Q

cycle of energy intake?

A

GI, liver, to adipose tissue and muscle tissue, where there is nutritional partitioning

336
Q

what three things influence individual predisposition to digestion?

A

genetics, early life events and epigenetics

337
Q

what neurotransmitters decrease food intake (3)

A

Norepi – Beta receptor; dopamine; serotonin

338
Q

what hypothalamic peptides decrease food intake (4)

A

Cordicotropin-releasing factor (CRF); urocortin; glucagon-like peptide I (GLP-I); cholecystokinin (CCK)

339
Q

peripheral factors that decrease food intake? 3

A

leptin, CCK, and insulin

340
Q

when are peripheral factor effects observed, that decrease food intake?

A

Leptin – long term signal; CCK – meal-related signal; insulin – effect observed after central administration

341
Q

central factors that increase food intake (6)

A

Norepi – alpha receptor; neuropeptide Y (NPY); melanin concentrating hormone (MCH); galanin; growth hormone-releasing hormone (GHRH); opioid peptides

342
Q

pereipheral factor that increases food intake (1)

A

hypoglycemia

343
Q

pathologies associated with food intake

A

obesity, anorexia nervosa, bulimia nervosa

344
Q

what fuels anabolism?

A

diet

345
Q

what processes happen during anabolism?

A

glycogen, triglyceride and protein synthesis

346
Q

what is anabolism?

A

making and storing compounds

347
Q

hormone profile of anabolism

A

insulin increase, glucagon decrease, GI peptide increase, leptin increase

348
Q

what fuels catabolism?

A

glycogen, fat deposits, muscle protein

349
Q

what processes happen during catabolism?

A

glycogenolysis, gluconeogenesis, lypolysis, ketogenesis, proteolysis

350
Q

catabolism hormone profile

A

insulin decrease, glugacon increase, catecholamines increase

351
Q

what two processes make glucose in liver?

A

glycogenolysis and gluconeogenesis

352
Q

what do muscles feed into gluconeogenesis?

A

amino acids and glycogen

353
Q

what does adipose tissue contribute to liver?

A

fatty acids

354
Q

what does liver do with fatty acids?

A

ketogenesis

355
Q

what is the result of ketogenesis?

A

ketones headed for nonCNS and CNS

356
Q

what is destination of glucose?

A

CNS

357
Q

What fuels CNS?

A

glucose

358
Q

most glucose transporters work by

A

facilitated diffusion

359
Q

why does glucose concentration outside of brain need to remain high?

A

because of concentration gradient needed for facilitated diffusion into brain

360
Q

what can be used by brain besides glucose

A

ketones

361
Q

name three substrates for glucogenesis

A

glycerol from lipolysis, pyruvate-lactate from muscle glycogen, amino acids from proteolysis

362
Q

where does glucose go once past the gut? (postmeal)

A

blood

363
Q

from blood where does glucose go?

A

muscle, liver, adipose tissue and nerve and other tissues

364
Q

what does blood glucose become in muscle?

A

glycogen

365
Q

what does blood glucose become in liver?

A

glycogen and triglycerides

366
Q

what does blood glucose become adipose tissue?

A

triglycerides

367
Q

how does glucose get to blood during fasting?

A

muscle and adipose tissue send amino acids, glycogen, and fatty acids to liver to become glucose through gluconeogenesis

368
Q

what do fatty acids become in liver?

A

ketones

369
Q

three types of cells in pancreas islets of langerhans

A

beta, alpha and delta cells

370
Q

beta cells

A

synthesis and secretion of insulin. Are in center of islet.

371
Q

alpha cells

A

25% of cell content in islets – make glucagon, periphery of islet

372
Q

delta cells

A

somatostatin producers in periphery of islet

373
Q

how are pancreas vascularized?

A

arterioles feed into center of islet so beta cells get exposed to high glucose concentration. Arterioles supply capillaries that drain into venules that drain out of islets.

374
Q

how are cells connected to one another in islets of langerhans?

A

by gap junctions so they can signal each other

375
Q

acinear cells

A

smaller than islet of langerhans cells (release into duodenum?)

376
Q

what is inside beta cells

A

high density of granules with insulin inside

377
Q

what increases insulin secretion?

A

amino acids, raised blood glucose, glucagon, gastrin, secretin, cck, GIP, sympathetic innervation (alpha-receptors), parasympathetic (cholinergic) innervation

378
Q

GIP

A

glucose dependent insulinotrophic peptide

379
Q

what is insulin secretion decreased by?

A

somatostatin, blood glucose, sympathetic innervation of beta receptros , stress (exercise, hypoxia, hypothermia, surgery, severe burns)

380
Q

how is response to orally administered glucose different from that delivered via IV?

A

greater insulin stimulating effect.

381
Q

how is response to orally administered aa different from that delivered via IV?

A

greater insulin stimulating effect.

382
Q

do peptides secreted by GI endo cells stimulate insulin secretion?

A

yes

383
Q

how does GLP-1 regulate insulin secretion and blood glucose levels?

A

Incretin and GLP-1 stimulate insulin release and inhibit glucagon release, both of which lower blood glucose

384
Q

what inactivates GLP-1?

A

DPP-4 enzyme

385
Q

what inhibits DPP-4? To what end?

A

drugs block DPP-4 and decrease glucose levels in blood

386
Q

where is GLP-1 secreted?

A

L-cells of GI

387
Q

how is an increase in blood glucose regulated?

A
  1. release of insulin 2. insulin binds to membrane receptors in liver cells, adipocyte and muscle cells 3. in liver, increase activity of glycogen synthase (stores glucose) and adypocyte and muscle, exocytosis and activation of glucose transporters (so glucose has where to go) 4. removal of glucose from blood and is stored as glycogen
388
Q

hos is decrease in blood glucose regulated?

A
  1. release of glucagon 2. glucagon binds to membrane receptor 3. activation of adenylyl cyclase 4. increase in cAMP, activation of cAMP-dependent kinase 5. activation of glycogen phosphorylase and inhibition of glycogen synthase 6. degradation of glycogen to glucose, release of glucose into blood
389
Q

subcellular sites of insulin biosynthesis in beta cells

A
  1. rough ER 2. microvesicles 3. golgi 4. early granules 5. mature granules 6. plasma membrane
390
Q

proinsulin to insulin process

A

86 aa proinsulin goes through protease and becomes 21 aa A-chain, 30 aa B-chain and C peptide

391
Q

what happens to glucagon in anticipation of oral glucose load?

A

its concentration initially increases, but then is suppressed by increase in insulin

392
Q

how does insulin react to oral glucose load?

A

rise in insulin lags behind glucose peak

393
Q

how does high glucose affect GH release?

A

high glucose suppresses basal GH release initially, but there is a surge after 2-3 hours. This is a response to falling glucose concentration.

394
Q

how do elevated insulin levels affect lipogenesis?

A

stimulate lipogenesis because it cases a decrease in circulating free fatty acids

395
Q

what does GH to to free fatty acids?

A

causes their release from adipose tissue for use by muscle and liver cells

396
Q

How does Glut2 transporter work?

A
  1. glucose enters cell via glut2 transporter 2. glucose metabolism produces ATP as it becomes pyruvate 3. ATP levels increase in cytoplasm and closes K+ channels 4. membrane depolarization follows causing step 5 5. opening of voltage gated Ca2+ channels 6. elevation oin cytosolic Ca2+ stimulates secretion of insulin.
397
Q

how does insulin receptor work?

A
  1. conformation change leads to receptor autophosphorylation and tyrosine phosphorylation of intracellular protein substrates 2. insulin activates 2 main branching pathways
398
Q

what two pathways does insulin receptor stimulate?

A

Ras-MAP kinase and IRS pathways

399
Q

Ras-MAP kinase pathway

A
  1. receptor binds Shc, which binds Grb2 ans SOS. 2. SOS binds Ras and Ras binds Raf 3. Raf activates MEK. 4 MEK activates Erk1/2, which causes cell proliferation and antiapoptosis
400
Q

what is Ras-MAP kinase pathway known as?

A

growth signal

401
Q

IRS pathway

A

actiavates kinase dependent on heterodimeric (p85/p110) p12K (protein kinase B). this modulates enzyme activities that control glucose, lipid and protein metabolism and affect NO generation and apoptosis. Also known as metabolic signal.

402
Q

how does insulin receptor signal transduction lead to metabolic changes

A

insulin binds and activates protein kinase B. protein kinase B activates Glut4 translocation and inactivates GSK3, which inhibits glycogen synthase

403
Q

what is insulin receptor like?

A

dimeric receptor tyrosine kinase

404
Q

what are two roles of insulin receptor?

A

Ras-MAP kinase pathway and glucose levels in circulation regulation

405
Q

What is IR made up of?

A

2 extracellular alpha subunits that bind insulin and 2 transmembrane beta-subunits that contain tyrosine kinase domain

406
Q

what mediates insulin effects on metabolism?

A

protein kinase B

407
Q

what does insulin result in with blood glucose?

A

increase of glucose transport from blood, translocation of glucose transporters to plasma membrane I fat and muscle, activation of glycogen synthase.

408
Q

how does glucose enter intestines and kidney?

A

secondary active transport with Na+

409
Q

how does insulin stimulate glucose entry into muscle, adipose and other cells?

A

upregulates no of glucose transporters in cell membrane

410
Q

where is Glut4 stored?

A

in muscle and adipose cells in vesicles in cytoplasm

411
Q

what happens to glut4 vesicles after insulin binds cell?

A

vesicles fuse with plasma membrand and increase no. of Glut4 on cell surface

412
Q

how does insulin affect liver catabolic pathways?

A

inhibits glycogenolysis, conversion of fatty acids and aa to keto acids and conversion of aa to glucose

413
Q

how does insulin affect liver anabolic pathways?

A

promotes glucose storage as glycogen (induces glucokinase and glycogen synthase, inhibits phosphorylase), increases triglyceride synthesis and VLDL formation

414
Q

how does insulin affect muscle protein synthesis?

A

increases aa transport, and ribosomal protein synthesis

415
Q

how does insulin affect muscle glycogen synthesis?

A

increases glucose transport, induces glycogen synthase, inhibits phosphorylase

416
Q

how does insulin affect adipose tissue triglyceride storage?

A

a. lipoprotein lipase is induced by insulin to hydrolyze triglycerides in circulating lipoproteins for delivery of fatty acids to adipocytes b. glucose transport nto cell provides glycerol phosphate to permit esterification of fatty acids supplied by lipoprotein transport c. intracellular lipase is inhibited by insulin

417
Q

how does insulin affect brain?

A

decreases appetite. Increases energy expenditure.

418
Q

how does insulin affect K+?

A

causes K+ to enter cells – lowers extracellular K+ concentration. Infusions of insulin and glucose lower plasma K+ level in normal individuals. Very effective for temporary relief of hyperkalemia in patients with renal failure. Increases activity of Na/K ATPase in cell membrane, so more K+ is pumped into cells

419
Q

how is glycogen synthesized?

A

UDP-glucose plus glycogen in residues , through glycogen synthase, results in glycogen (n + 1 residues) and UDP

420
Q

how is glycogen degraded?

A

glycogen (in residues) through glycogen phosphorylate and Pi becomes glucose-1-phosphate and glycogen (n-1 residues)

421
Q

how does increased cAMP regulate glycogen levels?

A

stimulates glycogen breakdown and inhibits glycogen synthesis. Inactive cAPK phosphorylates GPK, which phosphorylates GP, which breaks down into glycogen (n+1 residues) plues glucose. Inactive cAPK phosphorylates GS

422
Q

how does decreased cAMP regulate glycogen levels?

A

inhibits glycogen breakdown and stimulates glycogen synthesis. Active PP dephosphorylates GPK and GP and GS, which leads to UDP glucose becoming glycogen and UDP

423
Q

At what plasma glucose level does insulin secretion get inhibited?

A

Approx 80 mg/dL

424
Q

At what plasma glucose level do glucagon, epi, and GH get secreted?

A

Approx 68 mg/dL

425
Q

At what plasma glucose level is there cortisol secretion due to stress?

A

Approximately 55 mg/dL

426
Q

At what plasma glucose level is there cognitive dysfunction?

A

Approx 50 mg/dL

427
Q

At what plasma glucose level is there a coma?

A

30 mg/dL

428
Q

At what plasma glucose level are there convulsions?

A

20 mg/dL

429
Q

At what plasma glucose level is there permanent brain damage or death?

A

Under 15 mg/dL

430
Q

What is human proglucagon precursor to in alpha cells?

A

GRPP, glucagon, hexapeptide and major proglucagon segment.

431
Q

What is human proglucagon precursor to in small intestine?

A

Glincentin, Truncated GLP-1 and GLP-2

432
Q

What is Glincentin a precursor to?

A

GRPP and Oxyntomodulin

433
Q

What are steps of glucagon/receptor G-alpha-s pathway?

A

Glucagon binds with G protein 7 transmembrane domain. G alpha-s dissociates from Beta and gamma, loses GDP and gains GTP, and activates adenylate cyclase, which makes cAMP in cytoplasm. cAMP increases active PKA, which increases active phosphorylase kinase, which phosphorylates Phosphorylase, which increases glycogenolysis. Increase in active PKA also uses PGC-1, PEPCK and G-6-Pase to increase gluconeogenesis, which increases glucose.

434
Q

What are steps of glucagon/receptor G-q pathway?

A

G-q activates phospholipase C, which makes PiP2 and IP3, which leads to release of Ca2+ in cytosol, which leads to decrease in glycolysis and glycogenesis.

435
Q

What are the steps of glycogenolytic response stimulated by glucagon?

A

Glucagon activates adenylate cyclase, which makes cAMP, which activates phosphorylase kinase, which activates phosphorylase b to make it phosphorylase a, which accelerates the production of glucose-1-phosphate from glycogen.

436
Q

What regulates glycogen mobilization from the liver?

A

Glucagon

437
Q

By how much does glucagon accelerate production of glucose-1-phosphate from glycogen?

A

1000 fold

438
Q

is glycogen synthetase active or inactive in the phosphorylated form?

A

Inactive

439
Q

What does glucagon action on liver or epinephrine action on muscle stimulate?

A

Adenylate cyclase

440
Q

What kind of proteins are capable of phosphorylating glycogen synthetase?

A

Two protein kinases. One is cAMP dependent and the other cAMP independent.

441
Q

Glycogen synthetase regulation via glucagon and adreline.

A

Glucagon acts on liver. Adrenaline acts on muscle. Both hormones stimulate adenylate cyclase. Adenylate cyclase makes cAMP. cAMP activates cAMP-dependent protein kinase, which phosphorylates glycogen synthetase and renders it inactive.

442
Q

Glycogen synthetase regulation via insulin.

A

Insulin inhibits (somehow) cAMP-independent protein kinase, which makes it stop phosphorylating glycogen synthetase, so glycogen synthetase is activated because it has not be phosphorylated.

443
Q

How does insulin regulate glycogen synthetase via factor Fa?

A

Insulin activates Fa, which reacts with an inactive form of phosphoprotein phosphatase to produce the active form of the phosphatase. Phosphatase dephosphorylates glycogen synthetase, rendering it active.

444
Q

Percentage of adults in US with diabetes? Prediabetes?

A

11.3%/ 35%

445
Q

How does diabetes rank as cause of death in the US?

A

7th leading cause

446
Q

Insulin-dependent diabetes mellitus (IDDM)

A

Low or absent levels of circulating endogenous insulin; dependent on injected insulin to prevent ketosis and sustain life. Onset predominantly in youth but can occur at any age. Associated with certain HLA and GAD antigens. Abnormal immune response; islet cell antibodies are frequently present at diagnosis.

447
Q

Non-insulin-dependent diabetes mellitus (NIDDM)

A

Insulin levels may be normal, elevated, or depressed; hyperinsulinemia and insulin resistance characterize most patients and insulinopenia may develop as the disease progresses. Not insulin dependent or ketosis prone under normal circumstances but may require insulin for treatment of hyperglycemia. Onset predominantly after age 40 years but can occur at any age. Approximately 50% of men and 70% of women are obese. Cause probably strongly genetic; 60-90% of monozygotic twins are concordant for NIDDM.

448
Q

Gestational diabetes

A

Glucose intolerance that has its onset or recognition during pregnancy. Associated with older age, obesity, family history of diabetes. Conveys increased risk for the woman for subsequent progression to NIDDM. Associated with increased risk of macrosomia.

449
Q

Glucose pathway

A

Diet to intestine to plasma glucose. From blood goes to liver, muscle, adipose, brain and kidney. From kidney, glucose leaves through urine.

450
Q

Glycosuria

A

Glucose in urine

451
Q

What type of disease is Type 1 diabetes?

A

An autoimmune disease

452
Q

Pancreas/lymph node Type 1 diabetes pathway

A

Viral attack on pancreas, which release insulin pieces and other cell protein fragments that are taken to lymph nodes. Autorreactive T cells attack islet cells. Islet cells are killed.

453
Q

What happens to diabetics who have inherited DR3 (but not DR4)?

A

Tend to develop diabetes earlier in life and have an immune reaction against insulin.

454
Q

What happens to diabetics who inherit both DR3 and DR4?

A

They develop diabetes at the youngest age and have the highest levels of antibodies against insulin.

455
Q

Risk levels of HLA-DR allele 1-9

A

DR1 slight risk, DR2 protective, DR3 significant risk, DR4 significant risk, DR5 slight risk, DR6 neutral/protective, DR7 protective/risk in African descent, DR8 neutral/slight risk, DR9 risk in Chinese, Japanese, Korean descent

456
Q

What leads to type 2 diabetes?

A

Too much food/animal fat, not enough exercise, one set of genes inherited from parents make you hungry, another set of genes cause greater insulin resistance, being overweight, which makes body resistant to insulin, making it produce more

457
Q

How do genes affect pancreas directly in type 2 diabetes?

A

Make islet cells wear out early and one can’t make enough insulin.

458
Q

What do fatty deposits from being overweight do to pancreas?

A

Damage islet cells

459
Q

What is the cause of type 2 diabetes, insulin wise?

A

Body needs more insulin but can’t produce it

460
Q

How does body develop insulin resistance in type 2 diabetes?

A

Decrease in insulin receptor number, change in receptor signaling (from insulin R to GLUT4), decrease in the glucose transport

461
Q

How does abdominal adipose tissue change in obesity?

A

Macrophages and other immune cells change in obese fat tissue, and release elevated amounts of cytokines leading to metabolic disease. Immune cells cause low-grade inflammation, insulin resistance, and metabolic disease.

462
Q

How do insulin deficiency and glucagon excess contribute to underutilization of glucose?

A

Insulin very much. Glucagon zero.

463
Q

How do insulin deficiency and glucagon excess contribute to overproduction of glucose?

A

Insulin + Glucagon ++++

464
Q

How do insulin deficiency and glucagon excess contribute to increased glycogenolysis?

A

Insulin + Glucagon ++++

465
Q

How do insulin deficiency and glucagon excess contribute to increased gluconeogenesis?

A

Insulin + Glucagon ++++

466
Q

How do insulin deficiency and glucagon excess contribute to increased release of aa?

A

Insulin very much. Glucagon zero.

467
Q

How do insulin deficiency and glucagon excess contribute to increased release of aa?

A

Insulin very much. Glucagon zero.

468
Q

How do insulin deficiency and glucagon excess contribute to increased lipolysis?

A

Insulin ++++ Glucagon +

469
Q

How do insulin deficiency and glucagon excess contribute to increased hepatic ketogenesis?

A

Insulin + Glucagon ++++

470
Q

How does insulin deficiency lead to ketone acidosis?

A

Increase in lipolysis, increase in plasma free fatty acids, increase in ketone synthesis, increase in plasma ketones, increase in plasma H+ (acidosis), which leads to impaired brain function and death

471
Q

How does insulin deficiency lead to decrease in brain blood flow?

A

Decrease in glucose uptake by cells, increase in glycogenolysis and gluconeogenesis. Increase in plasma glucose. Increase in renal filtration of glucose and ketones. Osmotic diuresis. Increase in sodium and water excretion. Decrease in plasma volume. Decrease in arterial bp. Decrease in brain blood flow, which leads to impaired brain function and death.

472
Q

How does diabetes affect the vascular system?

A

Through atherosclerosis and arteriolosclerosis.

473
Q

Atherosclerosis

A

Of the aorta and large and medium-sized blood vessels leads to myocardial and brain infarctions and gangrene of the lower extremities.

474
Q

Arteriolosclerosis

A

Thickening of the wall of the arterioles; associated with hypertension

475
Q

How does diabetes affect the bladder?

A

Urinary bladder neuropathy (alteration in the autonomic nervous system)

476
Q

How does diabetes cause eye complications?

A

Total blindness. Retinopathy, cataract, glaucoma.

477
Q

Retinopathy

A

Damage of retina

478
Q

Cataract

A

Opacity of lens

479
Q

Glaucoma

A

Impaired drainage of the aqueous humor is frequently observed

480
Q

How does diabetes affect kidneys?

A

Glomerulosclerosis, aerteriosclerosis, pyelonephritis, and diffuse thickening of the basal lamina of the glomerular capillaries and proliferation of mesangial cells, or Kimmelstiel-Wilson lesion

481
Q

Gangrene

A

Caused by blood vessel obstruction as a consequence of vascular arteriosclerosis

482
Q

What causes osmotic damage in diabetes?

A

Increased activity of the sorbitol and glycogenic pathways

483
Q

What do glycosylation reactions in diabetes lead to?

A

Alterations in the eye and basement membranes of cells, which in turn affect permeability and transport mechanisms

484
Q

What does increase of glycogen in kidney and leucocytes cause?

A

Osmotic damage

485
Q

What kind of glycosylation of proteins happens in diabetes because of high circulating levels of glucose?

A

Non-enzymatic glycosylation

486
Q

Which amino acids are primarily glycosylated?

A

Lysine and valine

487
Q

What damage does diabetes do to eye?

A

Microaneurysms, “cotton wool” spots, hemorraghes, exudates and abnormal blood vessels.

488
Q

Difference between healthy and diabetic retinal capillaries.

A

Diabetic retinal capillaries – some are closed off, others form dilated segments “microaneurysms”

489
Q

What happens to basal lamina in diabetic kidney

A

Thickening

490
Q

What leads to neuropathy in diabetes?

A

Changes in nerve bundles (NB)

491
Q

Diabetes treatment options

A

Insulin pump, islet transplantation

492
Q

How does islet transplantation work?

A

Donor pancreas, isolate islets, use syringe to put islets in portal vein

Endocrinology (21 decks)

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