diabetes Flashcards

exam 4

1
Q

little to no insulin production

A

diabetes

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2
Q

hallmark of diabetes

A

hyperglycemia

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3
Q

treat type II diabetes and it is an alpha-glucosidase inhibitor

A

acarbose

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4
Q

acarbose works by

A

slowing down the enzyme that converts carbohydrates to sugar; thus results in smaller blood glucose rise

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5
Q

SGLT2 Inhibitor

A

Jardiance

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6
Q

Jardiance works by

A

stoping glucose absorption from nephron back to blood

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7
Q

Initial protein structure of insulin, _______ is made in ER lumen

A

pre-proinsulin

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8
Q

is excised and proinsulin is transported to Golgi

A

Signal peptide

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9
Q

C-peptide can be used to

A

assess whether β cells are producing insulin; if it is present in blood then that means insulin is also being secreted

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10
Q

In Golgi, proinsulin is converted to insulin by removal of ___________ and enters secretory granules

A

C-peptide

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11
Q

Glucokinase is present in the

A

liver and pancreas

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12
Q

ATP will bind and activate a _____ that results in depolarization → Ca2+ release → Insulin vesicle release

A

K+ Channel

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13
Q

Sulfonylureas and Meglitinides can control diabetes by

A

interacting at the ATP K+ Channel

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14
Q

__________are peptide hormones that work to INCREASE INSULIN SECRETION (augment its effect) → REDUCES GLUCOSE

A

Incretins

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15
Q

Incretins are made by endocrine cells of the small intestine

A

L-Cells create GLP-1

K-Cells create GIP

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16
Q

incretins act on ____ and why?

A

pancrease to drive insulin secretio

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17
Q

GLP-1 will bind to GLP-1R (GPCR) and activate

A

adenylate cyclase

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18
Q

cAMP activates PKA which acts on

A

K+ channel, allowing membrane depolarization, Ca2+ influx and insulin secretion

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19
Q

is a stable GLP-1/GIP analogue that will help augment insulin secretion and treat Type II Diabetes

A

Exenatide

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20
Q

is a Dipeptidyl Protease IV inhibitor, it binds and stops the enzyme that breaks down GLP-1/GIP

A

Sitagliptin (Januvia)

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21
Q

leads to ketoacidosis

A

Type I

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22
Q

HONC- hyperoamolar non-ketotic coma/HHS- hyperglycemic hyperosmolar syndrome

23
Q
  • Autoimmune reaction of -ABs to pancreatic β-cells
  • Normal response to insulin, BUT NO insulin production
  • Severe hyperglycemia
  • Genetic susceptibility
24
Q
  • Commonly seen with obesity
  • Preserved β-cells
  • Little to high insulin production; but usually REDUCED insulin response
  • Genetic susceptibility
25
can occur in some pregnancies; can cause effects in mother and child
Gestational Pregnancy
26
Insulin reduces blood glucose in 3 ways:
1. Causes translocation of GLUT4 receptors on muscle, fat, and white blood cells 2. Suppresses glycogenolysis 3. Suppresses gluconeogenesis
27
is a drug that interacts with COMPLEX I of ETC and cause the increased formation of AMP
metformin
28
AMP will bind to glucagon-receptor and
INHIBIT IT to prevent GLUCONEOGENIC PATHWAYS
29
Glucose reacts with metals to generate
reactive oxygen species
30
. The polyol pathway generates Sorbitol; the pathway will lead to an accumulate of Sorbitol which causes an
OSMOTIC EFFECT
31
Glycation generates protein adducts (HbA1c) leading to advanced ___________ (AGE) that are themselves reactive.
glycation endproducts
32
Can measure average blood glucose level with
HbA1c level
33
Polyol pathway consumes
NADPH
34
Insulin signaling involves
PROTEIN KINASE and LIPID SIGNALING
35
Insulin will bind to its receptor, which is a ____________; when insulin receptor is active it will phosphorylate ITSELF and ADAPTOR PROTEINS
tyrosine kinase
36
Ras will affect transcription factor kinases that will then cause changes in
transcription factors to drive gene transcription
37
p-IRS-1 will activate __________in protein kinase
Ras (GDP → GTP active)
38
Insulin-receptor will phosphorylate _________
IRS-1 (adaptor protein)
39
p-IRS-1 will activate __________in lipid signaling
will activate PI3 Kinase to cause formation of PIP3
40
PIP3 will cause activation of kinases such as______ and _____
PDK1 and AKT
41
Lipid signaling is responsible for
relocalization of GLUT4 transporter onto membrane of fat and muscle cells, which increases glucose uptake
42
Insulin resistance will cause what alterations in adipokines
adiponectin ↓ and resistin ↑
43
Adiponectin increases
insulin sensitivity
44
resistin increases
insulin resistance
45
Excess glucose is lost in urine, meaning there is
dehydration
46
No transport of glucose means glucose stays in blood; also continuous glycogenolysis and gluconeogenesis
hyperglycemia
47
A characteristic feature of diabetes is the LIPID TRIAD:
HIGH FAs, HIGH LDL, and LOW HDL
48
Normally, insulin will suppress ___________ and activates _______
suppress Hormone Sensitive Lipase and activates Lipoprotein Lipase
49
transfers lipids to adipose for storage
Lipoprotein Lipase
50
releases FAs from adipose in starvation
Hormone Sensitive Lipase
51
NO INSULIN means continuous release of fats from adipose due to ______ fats travel to the liver and are turned into ______
NO INSULIN means continuous release of fats from adipose due to HSL, fats travel to the liver and are turned into VLDL
52
HDL levels will decrease due to loss of
Apo-A1
53
Lungs and kidney respond to ACIDOSIS with
Kussmaul Breathing
54
Large amounts of FAs causes buildup of Acetyl-CoA in liver and thus __________ formation begins in the liver
ketone body