Week 7: Type 2 DM Flashcards

1
Q

DKA in which type of DM

A

Either Type 1 or 2 DM

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2
Q

Antibody testing negative for Type 1 or 2 DM

A
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3
Q

C-peptide testing for Type 1 or 2 DM

A
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4
Q

C-peptide testing

A

Injected insulin does not have C-peptide

Type 1 DM shouldn’t have C-peptide

if you don’t know what type of DM they have

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5
Q

Low C-peptide levels at Dx DM1 or DM2

A

could be either if DM1 in early Dx

DM2 late in Dx can be low

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6
Q

Epidemiology of DM

A
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7
Q

Increased adiposity in DM2

A
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8
Q

Type 2 DM mechanism

A

increased adiposity

increased energy intake

ectopic FAs accumulation

so what happens is there are breakdown products from FA deposition and interfere with insulin signaling leading to insulin resistance and can lead to DM2

ability for pancreas to keep up with excess insulin secretion can decrease leading to DM2

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9
Q

Risk for DM2

A
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10
Q

Methods for Dxing DM2

A
  • Fasting glucose level (1 day)
  • oral glucose tolerance (1 day)
  • HbA1c (~ 3 months) (glycosylated Hb)
    *
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11
Q

Diagnostic criteria for DM2

A

Also random glucose of >200 mg/dL

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12
Q

Treatment options for DM2

A
  • Metformin

w/ Heart disease

  • SGLT-2 inhibitors
  • GLP-1 inhibitors
  • TZDs
  • Sulfonylureas
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13
Q

1st line therapy for DM2

A

Metformin

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14
Q

Metformin Effects

A
  • Suppresses hepatic glucose production (gluconeogenesis)
  • Increase insulin sensitivity
  • Increase peripheral glucose uptake
  • Decrease GI absorption of glucose
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15
Q

Metformin Side effects

A

GI intolerance/Diarrhea

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16
Q

Natural history of DM

A

aging is a bitch

17
Q

SGLT-2 Inhibitors effects

A

inhibits SGLT-2 channel in the proximal tubule of the nephron

prevents reabsorption of Glucose and Na

loses calories in the urine and diuretic effect for blood pressure

18
Q

List of SGLT-2 Inhibitors

19
Q

GLP-1 Agonists effects

A

Normally when we eat carbohydrates the L cells of the small intestines secrete GLP-1 and it acts on a variety of receptors

GLP-1 receptors in the:

  • β cells of the pancreas ((augment glucose-dependent insulin secretion *only increased insulin secretion during meals preventing low blood sugars* unlike sulfonylureas)
  • Alpha cells of the pancreas (reduce postprandial glucagon secretion reducing glucose output from the liver)
  • Stomach (slows down emptying of the stomach helping them feel full sooner and also slows down the absorption of carbohydrates)
  • CNS (promotes satiety and reduces appetite)

Glucose lowering and reduction of weight

Don’t see a lot of hypoglycemia,

20
Q

GLP-1 Agonists Side effects

21
Q

Caveat of GLP-1 agonists

A

When GLP-1 is secreted from the small intestines, it is rapidly inactivated by DPP-4

GLP-1 agonists are resistant to DPP-4 degradation)

22
Q

DPP-4 inhibitors

A

inactivate DPP-4 preventing the inactivation of endogenous GLP-1

don’t see a lot of hypoglycemia

23
Q

List of GLP-1 agonists

24
Q

List of DPP-4 inhibitors

25
TZDs AKA
Thiazolidinediones
26
TZDs effects
Stimulate nuclear PPARγ receptors causes enhanced insulin sensitivity
27
TZDs side effects
Risks of weight gain, fluid retention, fractures
28
Names of TZDs
Pioglitazone
29
DM that promote weight loss
GPL-1 agonists SGLT-2 inhibitors
30
DPP-4 inhibitors and weight
actually weight neutral
31
Sulfonylureas effects
help the pancreas make more insulin Glucose in glucose transporter and glycolysis and TCA to generate ATP ATP less K+ leaves islet cell and depolarizes cell and voltage-gated Ca2+ channel opens causing Ca2+ influx and causes insulin exocytosis and secretion Sulfonylureas inhibits the K+ channel in substitution of ATP to cause depolarization and insulin secretion Problem is that it doesn't matter if the patient is eating or not
32
Sulfonylureas side effects
* hypoglycemia * Weight gain
33
Sulfonylureas benefits
improved glucose control
34
Sulfonylureas MOA
Stimulate pancreatic insulin secretion by K+ leak channel inhibition
35