Pcol Test 1 Diabetes Packet

Front 1

what are the symptoms of type 2 diabetes

Back 1

polydypsia, polyuria, elevated glucose, elevated insulin, proteinuria, obesity (unless MODY), ketonuria (only if insulin has diminished)

Front 2

what do FFA and soluble factors do to the liver

Back 2

they cause hepatic signaling dysfunction

the visceral adipose tissue secretes FFA that favor gluconeogenesis and they impair fat storage so instead of storing our excess glucose by converting it to lipids the liver secretes FFA

Front 3

what does FFA and high glucose do to the pancrease

Back 3

less storage of glucose in adipose tissue
since there is less insulin fxn there is no suppression of (ketogenesis, glycogenesis, lipogenesis, gluconeogenesis)

since there is less insulin glucagon secretions are no longer suppressed

pancreatic Beta cell death due to high glucose and FFA

Front 4

what is the main stimulant of gluconeogenesis

Back 4

glucagon

Front 5

how do high glucose and FFA cause pancreatic Beta cell death

Back 5

since there is a such a high concentration of glucose it will eliminate many of the reducing equivalents which usually take care of free radicals therefore these free radicals will damage the cells in the pancreas

Front 6

where is visceral fat found

Back 6

fat deposits in the organs

Front 7

what do FFA and souluble factors do to skeletal muscle

Back 7

TNF alpha causes the myoctes to become resistant to insulin therefore we can't take up glucose into skeletal muscle causing our blood glucose to increase

Front 8

what is the normal insulin pathway

Back 8

insulin binds to insulin receptor

conformational change activates the Tyrosine Kinase

insulin receptor substrate gets phosphorylated

IRS recruits PIK3

PIK3 activates PKB

PKB fascilitates the translocation of GLUT4 to cell membrane

Front 9

what is the pathway seen in someone that is insulin resistant/hyperinsulinemia

Back 9

insulin will bind to IGF Rc

IGF Rc autophosphorylates and activates PKC

PKC goes to the insulin receptor and inactivates it by phosphorylating the serine and threonine

this results in GLUT 4 not being translocated into the membrane

Front 10

what also activates PKC

Back 10

TNF ALPHA

Front 11

what do soluble factors and FFA do to the liver, muscle, and pancreas

Back 11

interfer with insulin signaling in the liver (instead of storing glucose, and storing lipids in adipose tissue, we're making glucose and secreting FFA)

cause pancreatic beta cell death in the pancreas (this is due to the high amount of glucose and FFA)

increase insulin resistance in the muscles (mainly due to TNF alpha)

Front 12

what kind of kinases are PKB/PKC

Back 12

serine thereonine kinases

Front 13

what all does TNF alpha do

Back 13

activate PKC
increase lipolysis in adipose tissue
interfere w/ skeletal myocyte insulin signaling

Front 14

why is exercise recommended for diabetes

Back 14

muscle contraction causes glycolysis, generation of lactic acid, make and consume ATP, and generate heat

when ATP is used we end up with AMP

AMP kinase gets activated by increase in temp, demand for ATP, and decreased pH (lactic acid)

THIS LEADS TO INSULIN INDEPENDENT GLUCOSE TRANSPORT WHICH OCCURS EVEN IF WE'RE INSULIN RESISTANT

Front 15

what inhibits AMP kinase

Back 15

hyperglycemia

Front 16

what does AMP kinase do in the muscle, liver, adipose tissue

Back 16

in the muscle it would lead to the activation of IRS which would carry out its pathway leading to GLUT4 translocation. THIS IS DONE W/O INSULIN

in the liver AMP kinase causes gluconeogenesis

in adipose tissue AMP Kinase INCREASES LEPTIN (decrease apetite)
INCREASES LIPOGENESIS (store fat)
INCREASES FFA OXIDATION (burn fat)
INCREASES GENE EXPRESSION OF ADIPONECTIN GENE (circulating adiponectin activates AMP kinase in the liver and muscle)

Front 17

what does adiponectin do when it gets to skeletal muscle or the liver

Back 17

activates AMP kinase

Front 18

what do alpha glucosidase inhibitors do

Back 18

THEY DELAY RATHER THAN INHIBIT CARB UPTAKE by inhibiting alpha glucosidase

Front 19

what do you treat people w/ if their insulin release is sluggish

Back 19

insulin secretogoges

Front 20

what are the insulin secretegogues

Back 20

meglitinides (repa/nate), sulfolnylureas, incretins

Front 21

what do you treat hepatic signaling dysfunction with

Back 21

biguanides (metformin) because they decrease hepatic glucose synthesis and have a minor effect of increases glucose uptake in the guy

Front 22

what do you treat myocite insulin resistance with

Back 22

TZD

Front 23

what are the side effects of alpha glucosidase inhibitors

Back 23

flatulance, ab pain, diarrhea

Front 24

what drug has an expected side effect of hypoglycemia

Back 24

sulfonylureas

Front 25

what do sulfonylureas do

Back 25

stimulate preformed, stored, insulin release

they bind to and inhibit the ATP dependent K channel via SUR Rc

Front 26

what do meglitinides do

Back 26

close ATP dependent K channel
PREPRANDIAL USE (right before meal)
GLUCOSE DEPENDENT
don't see hypoglycemia (won't work in people w/ normal blood sugar)

Front 27

what is an example of a Biguanide

Back 27

Metformin (glucophage)

ACTIVATES AMP KINASE

Front 28

why does pioglitizon have a better lipid profile

Back 28

because it has both PPAR alpha and gamma activity

rosiglitizone only has gamma

Front 29

how do TZD work

Back 29

they regulate a variety of insulin responsive genes

Front 30

what are the properties of PPAR gamma 2

Back 30

important for adipocyte differentiation and development

regulates adiponectin and leptin

Front 31

where is the PPAR Rc found

Back 31

adipose tissue, endothelial cells, myocytes, blood monocytes, all vascular smooth muscle

Front 32

what is a analog of amylin

Back 32

Pramlitinide

Front 33

what are the properties of Pramlitinide

Back 33

satiety factor
slows gastric emptying (allowing for better control of blood glucose b/c slows down the amount reaching the intestine and blood stream)

Front 34

what all does amylin do

Back 34

inhibits glucagon
slows gastric emptying
suppresses insulin release
decrease apetite

NET EFFECT OF LOWERING POST PRANDIAL GLUCOSE AND SLOWING GLUCOSE ENTRY INTO BLOOD STREAM

Front 35

what does Exenatide do and what is its generic name

Back 35

Byetta

acts like GLP1 therefore it is a satiety factor, may increase beta cell mass, and promotes insulin release

Front 36

what do DPP IV inhibitors do

Back 36

can reduce post prandial and fasting blood glucose

all it does is allow us to maintain incretins for longer

GIVEN ORAL ONCE A DAY

Front 37

what is an example of a DPP IV inhibitor

Back 37

sitagliptin (januvia)

Front 38

what can sitagliptin be given in combination with

Back 38

metformin and PPAR

Front 39

what lowers HB1Ac

Back 39

TZD

Front 40

what does metformin do to the weight

Back 40

neutral

Front 41

what does exenatide do to the weight

Back 41

weight loss

Front 42

what does TZD do to weight

Back 42

increase

either store when insulin is more responsive or fluid retention may occur