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ENR Biweekly 3 > Kauflers- Pancreatic Hormone Secretion > Flashcards

Kauflers- Pancreatic Hormone Secretion Flashcards

1
Q

retroperitoneal structure; if a cancer is growing there you won’t notice until too far advanced due to no sensation of pain

A

pancreas

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2
Q

Pt will have severe pain and vomiting every time they try to eat something. Usually presents in young adults who are accused of having an eating disorder

A

SMA syndrome

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3
Q

what supplies pancreas

A

splenic a. and SMA

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4
Q

blood from pancreas drains where

A

into portal vein

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5
Q

where does pancreas come from embryologically

A

foregut and endoderm

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6
Q

when the buds don’t rotate so they don’t fuse correctly, and the pancreas is wrapped around duodenum and traps it, causing duodenal obstruction

A

annular pancreas

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7
Q

If mom has uncontrolled diabetes, all her extra blood sugar will cross the placenta and the baby will start cranking out excess insulin in response (extra insulin makes you bigger). This will make the baby really really ______, even before birth

A

fat

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8
Q

clusters of endocrine cells of pancreas

A

Islets of Langerhan’s

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9
Q

main location of Islets of langerhans

A

tail of pancreas

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10
Q

____ cells of pancreas get the most blood flow

A

beta cells

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11
Q

glucagon is made from what cells

A

alpha cells

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12
Q

insulin is made from what cells

A

beta cells

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13
Q

somatostatin is made from what cells

A

delta cells

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14
Q

pancreatic polypeptide is made from what cell

A

F cells

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15
Q

_____diabetes is caused by autoimmune destruction of the beta cells inside the islets. The B cells fill up with bad lymphocytes, then suffocate and die

A

type I

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16
Q

steps of actual insulin synthesis

A

Preproinsulin
proinsulin
insulin + C-peptide

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17
Q

mature insulin is made up what chains

A

alpha and beta (connected by disulphide bonds)

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18
Q

synthetic insulin made by drug companies does not contain what

A

C-peptide

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19
Q

how does glucose from the blood enter pancreatic beta cell

A

GLUT2 transporter

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20
Q

how insulin gets out of beta cell

A

glucose comes in
ATP is made
K+ channels close
Ca2+ channels open
release of insulin and C-peptide

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21
Q

drugs that make K+ channels close and cause insulin release

A

Sulfonylurea drugs

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22
Q

newborn w/ high blood sugar at birth due to K+ channels unable to close in beta cell and no release of insulin

A

monogenic (neonatal) diabetes

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23
Q

newborn born with low blood sugars due to excessive insulin release (K+ channels stay shut)

A

congenital hyperinsulinism

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24
Q

drug that doesn’t let K+ channels close and treats congenital hyperinsulinism

A

Diazoxide

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25
Q

marker of beta cell function

A

C-peptide

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26
Q

type I or type II diabetes how to distinguish

A

C-peptide low in type I and high in type II

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27
Q

Insulin high, C-peptide low

A

patient given exogenous insulin

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28
Q

Exogenous insulin injection will have _____ C-peptide

A

low

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29
Q

Insulin tumor (insulinoma) will have ____ C-peptide

A

high

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30
Q

most powerful stimulus for insulin release

A

blood glucose level

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31
Q

______ causes high BG, which causes insulin release

A

glucagon

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32
Q

hormone made by the gut when you eat and stimulates insulin release

A

GLP-1

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33
Q

______ nerve activation stimulates insulin release

A

vagal

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34
Q

_____-adrenergic stimulation stimulates insulin release

A

beta2

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35
Q

This medication turns off Dopamine in the brain, which turns off sympathetic nerve stimulation. When the sympathetic nerves are deactivated, they can’t inhibit insulin release, so more insulin is made by the beta cell
(antagonist for D1 and agonist for D2)

A

Bromocriptine

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36
Q

_____-adrenergic stimulation inhibits insulin release

A

alpha-adrenergic

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37
Q

Epi and NE bind _____ that inhibits insulin release

A

alpha adrenergic receptor

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38
Q

____ inhibits insulin release (also turns everything off)

A

somatostatin

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39
Q

____ hormone inhibits insulin release; why it causes elevated blood sugar levels

A

growth hormone

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40
Q

anti-inflammatory and immune suppressive drug that inhibits insulin release

A

glucocorticoids

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41
Q

what two ways to make insulin last longer in the blood

A

IV drip and subcutaneous injection

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42
Q

for type I diabetics, type of insulin shot that provides a continuous supply of low-dose insulin for 24 hours

A

basal dose of insulin

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43
Q

_______ dose of insulin, every time they eat, so that they can get a TON of insulin for the food. (lasts a couple of hours); ton of insulin at first in the first few minutes and second phase of release over about an hour or so to pick up the rest of sugar

A

bolus dose of insulin

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44
Q

the two phases of insulin release after food is messed up in type ___ diabetes

A

2

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45
Q

these patients have a lowered first phase and exaggerated second phase
(their beta cells are tired)

A

type 2 diabetics

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46
Q

low blood sugar feel the effects hours later for eating _______; body got rid of sugar by kidneys and others, and then insulin kicked in after and now low blood sugar

A

cake

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47
Q

Go LOW with ______ if you have type I diabetes, b/c basal rate keeps going on your pump, and your liver turns off!!!!!! (so no glucagon can act on it)

A

alcohol

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48
Q

Go LOW if you _____ eating, basal rate keeps going, and liver stops making sugar

A

stop eating

49
Q

If you are making too much growth hormone because you have a growth-hormone making tumor, then you ______ the insulin receptors, which can lead to high blood sugars

A

down-regulate

50
Q

Too much insulin (Type 2 diabetes), Obesity (eating lots of sugar which leads to too much insulin being made), and excessive growth hormone* will _____ the insulin receptors

A

hide (insulin resistance)

51
Q

_______and ______ will increase the insulin receptors, which leads to improved “insulin sensitivity”

A

exercise and not eating

52
Q

without ____receptors on surface of cell, glucose cannot be brought in from the blood

A

insulin

53
Q

______ in the blood binds to the alpha parts, which causes the autophosphorylation of the tyrosine residues on the beta parts on the inside of the cell

A

insulin

54
Q

beta parts of insulin receptor have _______ activity

A

tyrosine kinase

55
Q

what 2 pathways are activated when tyrosine proteins get phosphorylated (insulin receptor substrates)

A

PI3K and MAPK

56
Q

what does PI3K do

A

tell GLUT4 transporters

57
Q

In ______, the GLUT 4 transporters never get the signal to turn on (another side effect of insulin resistance). If they don’t get turned on, then they don’t go pull any glucose out of the blood. The result is that the patient has high blood sugar, and no energy for the muscles, so they are too tired to exercise, then eat more chips, which makes insulin resistance worse

A

type 2 diabetes

58
Q

GLUT transporter on beta cells

A

GLUT2

59
Q

GLUT transporter on skeletal muscle cells and adipose tissue

A

GLUT4

60
Q

anabolic hormone that will bulk you up

A

insulin

61
Q

_____ store glucose as glycogen for their own fuel when they need it (bulks up muscle)

A

muscles

62
Q

______ pathway also is involved in cell growth and transmits a strong anti-apoptotic signal, promoting cell survival

A

PI3K

63
Q
A

acanthosis nigricans

64
Q

dark velvety patches on the back of the neck, which indicates insulin resistance, or excessive amounts of insulin in the blood. Insulin increases the growth of keratinocytes on the skin and prevents their death

A

acanthosis nigricans

65
Q

pathway responsible for the growth-promoting effects of insulin

A

MAPK pathway

66
Q

induces storage of energy (glucose)

A

insulin

67
Q

tells your liver, muscle, and fat cells to store glucose and don’t let it get turned into energy

A

insulin

68
Q

insulin causes _______blood levels of:
Glucose
Free fatty acids
Ketoacids*
Amino acids

A

decreased

69
Q

how to treat DKA

A

give insulin to get rid of ketones

70
Q

Immediate response, within seconds of binding to the _______receptor:
Tells potassium and glucose to enter the cells, and get out of the blood

A

insulin

71
Q

how insulin has activation effects on the liver

A

promotes glycogen synthesis
promotes triglyceride, fatty acid, protein synthesis

72
Q

how insulin inhibits the liver

A

inhibits breakdown of glycogen
inhibits gluconeogenesis
inhibits breakdown of FA’s, AA’s, and ketogenesis

73
Q

insulin’s activating effects on muscle

A

increases glucose uptake
promotes glycogen synthesis
protein synthesis
increases K+ uptake

74
Q

insulin’s inhibiting effects on muscle

A

decreases protein degredation
inhibits breakdown of glycogen

75
Q

insulin’s activating effects on fat

A

increases glucose uptake
promotes TG, FA synthesis
increases K+ uptake

76
Q

insulin’s inhibiting effect on fat

A

decreased lipolysis

77
Q

GLUT transporter in hepatocytes

A

GLUT 2

78
Q

cells of nervous system mostly use GLUT _____

A

GLUT 3

79
Q

insulin dependent glucose transporter

A

GLUT 4

80
Q

responsible for facilitated diffusion of glucose across the cell membrane

A

GLUT

81
Q

are responsible for the secondary active transport of glucose in the intestine and renal tubules

A

SGLT

82
Q

stop glucose reabsorption in the kidneys; also help reduce blood pressure

A

SGLT2 inhibitors

83
Q

GLUT transporter for brain and erythrocytes

A

GLUT 1

84
Q

beta cells of pancreas and liver GLUT transporter

A

GLUT 2

85
Q

most neurons have _____ GLUT transporters

A

GLUT 3

86
Q

GLUT transporter for muscle and fat tissue

A

GLUT 4

87
Q

GLUT transporter for sperm

A

GLUT 5

88
Q

transporter of glucose in small intestine and renal tubules

A

SGLT1

89
Q

transporter of glucose in renal tubules

A

SGLT2

90
Q

In normal people, the SGLT2 will stop grabbing sugar if the blood sugar is above _____ mg/dl, and therefore the patient will spill glucose into the urine.

A

180

91
Q

-GLIFLOZINS

A

SGLT2 inhibitors

92
Q

synthesis of glucagon

A

proglucagon
glucagon
(in alpha cells)

93
Q

in the GI tract, alpha cells start making Proglucagon and then processed into _____ instead of glucagon

A

GLP-1

94
Q

_____ produced in response to a high concentration of glucose in the gut, such as after you eat a bunch of sugar

A

GLP-1

95
Q

____goes over to the beta cells in the pancreas and increases insulin release

A

GLP-1

96
Q

incretin – a group of gut hormones that augment insulin release after a high-sugar meal*
Feel fuller longer and eat less food

A

GLP-1

97
Q

low blood sugar
high AA’s levels
beta2 adrenergic stimulation
vagal stimulation
stress (cortisol)
epi
(cause what)

A

causes release of glucagon

98
Q

high blood sugar
somatostatin
insulin
alpha-adrenergic stimulators
(cause what)

A

causes inhibition of glucagon

99
Q

what doesn’t respond to glucagon after drinking (in type I diabetes, pump is still going and liver is not on, seizure due to insulin being given with no sugar —–low blood sugar seizure )

A

the liver

100
Q

what to do if type 1 friend is hypoglycemic after a night of drinking

A

give her honey or sugar on the inside of cheek

101
Q

_____ has tyrosine kinase receptors

A

insulin

102
Q

_____ has GPCR

A

glucagon

103
Q

promotes glucose synthesis and inhibits its breakdown

A

glucagon

104
Q

____ and ____ breakdown triglycerides and glycogen in muscle

A

glucagon and epinephrine

105
Q

causes high blood sugar but also stimulates secretion of the things needed to bring blood sugar down so they can be on call when ready to act

A

glucagon

106
Q

what happens in starvation

A

first 3 days glucagon tells liver to break down glycogen stores and make glucose
then, ketones and FA’s become main source of energy
after all fat is burned off, body breaks down muscle, using proteins for energy

107
Q

causes an increase in glucagon, which increases glucose production, to keep the blood glucose level stable

A

exercise

108
Q

ratio is ___ b/t insulin and glucagon if you eat a balanced diet

A

2

109
Q

best diet to eat to maintain a good blood glucose level

A

high protein and low carbs (protein will not have as much glucose being stored so won’t gain weight as quick)

110
Q

turns off everything

A

somatostatin

111
Q

glucose, AA’s, FA’s, gastric hormones, and glucagon stimulate what release from delta cells

A

somatostatin

112
Q

what blocks somatostatin release

A

insulin

113
Q

Parathyroid tumors (high calcium)
Pituitary tumors (could be excess GH or prolactin)
Pancreatic tumors

A

multiple endocrine neoplasia type 1 (MEN1)

114
Q

made by F cells and slows absorption of food; regulates hunger and absorption of food

A

pancreatic polypeptide

115
Q

___ release is stimulated by these things

A

pancreatic polypeptide

116
Q

what inhibits pancreatic polypeptide release

A

somatostatin

117
Q

made by beta cells and augments insulin; helps insulin control blood sugar, turns off glucagon, and slows gastric emptying

A

Amylin

118
Q

slowing _____ causes less sugar to get absorbed too quickly and weight gain; prevents hypoglycemia

A

Amylin

119
Q

these 2 levels are low in type 1 diabetes

A

Amylin and C-peptide

ENR Biweekly 3 (14 decks)

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