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diabetes Flashcards

1
Q

diabetes mellitus

A

metabolic disease that causes high blood glucose

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2
Q

type I diabetes

A

don’t make insulin. insulin-dependent diabetes mellitus
autoimmune destruction of pancreatic beta cells

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3
Q

discovery of insulin

A

blocked pancreatic ducts till acini cells degenerated leaving islets(pancreatic beta cells/insulin)

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4
Q

successful treatment of depancreatized dogs w ____

A

Isletin

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5
Q

type II diabetes

A

noninsulin-dependent diabetes mellitus, 90% of diabetes in the U.S., largest risk factor is obesity

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6
Q

physiological mechanism of glucose

A

carbs broken down into glucose by glucosidase –> pancreatic beta cells where ATP –> insulin secretion

insulin can also go to muscle cells –> glycogen or fat (adipose) cells –> triglycerides where PPARgamma cells help promote glucose storage as triglyceride or liver cells –> glycogen

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7
Q

glucagon

A

converts glycogen back into glucose, and causes gluconeogensis

GLP-1 analogue
DPP inhibitor

metformin and ozempic inhibit this!

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8
Q

type of channel on pancreatic cell and mechanism

A

potassium/ATP channel where glucose comes through and turns into ATP, ATP inhibits the channel and the cell is depolarized bc potassium channel is closed, calcium comes in and insulin is released

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9
Q

insulin is a ___ amino acid protein, made in the ___ and exported to the _______, where it is cleaved at various sites and releases __ peptide

A

51; endoplasmic reticulum; golgi apparatus; c peptide

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10
Q

in the golgi, insulin forms a hexameric struture with ____

A

zinc

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11
Q

hexameric structures do/do not cross membranes easily

A

do not, bc insulin hexamers have to break down into monomers to diffuse rapidly

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12
Q

Lispro insulin

A

breaks down more easily and is taken up into the body more quickly, this is a derivative of insulin made with other amino acids?

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13
Q

insulin receptors are found . . .

A

on surface of all target cells, esp. liver, muscle, adipose

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14
Q

insulin receptors and mechanism

A

receptor w tyrosine kinase domains, 2 beta subunits 2 alpha subunits and when insulin binds, it activates the receptor. the kinase gets activated and phosphorylates the tyrosine on the subunits – phosphotyrosine which is important for downstream signaling, recruits other proteins like IRS proteins (scaffold proteins), which recruit more proteins and get sifgnaling complex

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15
Q

liver

A

increased glucokinase activity

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16
Q

skeletal muscle and adipose tissue

A

stimulate translocation of GLUT4

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17
Q

IRS proteins also activate ___ pathway

A

Ras (g protein), creates more hexokinase

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18
Q

PI3Kinase –>

A

PIP3, which phosphorylates PKB –> glucose transporters inserted into membrane –> glucose taken into muscle –> glycogen synthase stores it into glycogen

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19
Q

insulin promotes the storage of glucose into ____

A

glycogen

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20
Q

glycogen synthase regulated by

A

GSK-3beta, which is normally active

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21
Q

how does insulin regulate synthesis of glycogen

A

increasing glucose transporters so that the liver can take up more glucose, and inhibiting GSK 3 beta to store glucose into glycogen

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22
Q

glucagon and epinephrine

A

make more glucose

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23
Q

insulin in muscle cell

A

glucose –> glycolysis –> krebs cycle –> triglycerides and ATP, and protein production

24
Q

type i diabetes

A

glucagon, epi, etc. will stimulate liver to make even more glucose making the situation worse! glucagon, catecholamines, glucocorticoid all inhibit insulin action, leading to more glucose

25
liver under goes gluconeogensis and ________ which dumps even more glucose into blood
glycogenolysis
26
ketones are made how
liver - breakdown of fatty acids from the adipose tissue into ketone bodies --> diabetic ketoacidosis
27
blood glucose levels sxceeds the kidneys ability to reabsorb glucose from
glomerular filtrate
28
osmotic diuresis
polyuria and polydipsia (thirst)
29
onset of type I
often in childhood or adolescence, destruction of beta cells is gradual but onset of disease is sudden (beta cells will provide sufficient insulin until approx. 85% are destroyed)
30
genetic predisposition of type i
alleles on chromosome 6 - code for HLA(human leukocyte antigens)
31
therapy for type I
exogenous insulin, just giving back insulin
32
complications
type I - ketoacidosis - rapid coma and death type I and II - altered mental status bc of hyperosmotic syndrome- confusion chronic - premature atherosclerosis, retinopathy (increased blood glucose damages blood vessels that feed the retina NPDR - nonproliferative diabetic retinopathy, and blood vesels leak fluid causing retina to swell and vision to blur, or proliferative diabetic retinopathy where abnormal blood vessels grow on the surface of the retina disrupting nomrla blood flow and may pull on retina causing it to detach), nephropathy, and neuropathy (nerve damage that causes numbness in extremities) diabetics are 2-4 times more likely to have heart disease
33
normal BGL
between 70 mg/dl and 110 mg/dl
34
how to assess blood glucose
acutely - BGL monitor chronically - glycohemoglobin - HbA1c levels over 7.5% diabetic
35
insulin preparations
regular (crystalline zinc, delayed absorption due to hexamer formation), NPH (neutral protamine Hagedorn, protamine binds to insulin and lowers solubility), Lispro,
36
Insulin analogues
aspart, lispro, glulisine, glargine
37
insulin pumps
dexcom; continuous glucose monitor
38
pathophysiology of type 2 DM
diet, exercise, weight control, race, heredity, age, insulin resistance
39
adipose cells full of
macrophages, which release cytokines
40
cytokines activate
JNK, which phosphorylates a ser on IRS1, so then IRS1 cannot get downstream molecules, you block downstream signaling
41
adiponectin enhances
insulin sensitivity; fat mouse example, released from fat cells - AMPK - fatty acid oxidation -
42
thiazolidinedione drugs activate PPARgamma , which increase
fat cell number and size, and adiponectin
43
type ii diabetes therapy
alpha-glucosidase inhibitors to slow glucose absorption in GI tract, sulfonylureas and meglitinides to increase beta cell secretion, thiazolidinediones and biguanides (metformin) to increase insulin sensitivity at target tissues
44
biguanides
metformin
45
metformin mechanism
decrease ATP levels in mitochondria to activate AMPKinase, changing ratio of ATP to AMP, --> inhibits expression of enzymes that are involved in the synthesis of glucose, reducing glucos, also phosphorylates the enzyme that makes fat --> breaks down more fats???
46
metformin side effects
diarrhea, nausea, back pain, muslce pain cramping
47
sulfonylureas
1st gen - weight gain tolbutamide 2nd gen - glyburide, glipizide block potassium channel to release more insulin
48
TZDs/glitazones
PPAR-g agonist, stimulate the production of adiponectin
49
alpha-glucosidase inhibitors
competitively inhibit alpha glucosidase enzymes in brush border of small intestine and pancreatic alpha amylase, delay brekadown of carbohydrates into glucose. (oligosaccharides to monosaccharides)
50
GLP-1 and the incretin effect
oral glucose increase - incretin effect GLP-1 secreted from intestinal cells --> release of insulin from beta cells, and decrease glucagon, reducing hepatic glucose output, slows gastric emptying, reduces appetite very short half life
51
sitagliptin mechanism
inhibit enzyme to increase levels of GLP-1 (DPP-IV inhibitor)
52
lizard spit
exenatide, more than 50% overlap with human GLP-1 byetta
53
glp1 receptor agonsits
stimualte insulin secretion after elevaeted flucose, everything glp1 does and weight loss ozempic
54
SGLT2 inhibition
invokana, farxiga block SGLT2, block transporter and get rid of glucose!
55

pharmacology (10 decks)

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