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3b_Boards - SketchyPharm > (5) GI & Endo: DM (2.1-2.2) > Flashcards

(5) GI & Endo: DM (2.1-2.2) Flashcards

1
Q

Stimulation of what adrenergic receptor increases insulin secretion?

A

β2

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2
Q

How does glucose induce insulin release?

A

Closes ATP dependent K+ channels

↑ Glucose

⇒ ↑ Aerobic respiration

⇒ ↑ ATP

⇒ Closure of ATP gated K+ efflux channels

⇒ ↑ Membrane voltage

⇒ Opening of voltage gated Ca2+ channels

⇒ Ca2+ influx

⇒ Exocytosis of insulin

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3
Q

Name 2 proteins secreted from the same vesicle as insulin

A

(1) C-peptide
(2) Amylin
* (Note: C-peptide is not included in exogenous insulin ∴ C-peptide can be used as a marker for insulin poisoning)*

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4
Q

What class of receptor is the insulin receptor?

A

Intrinsic receptor tyrosine kinase

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5
Q

What receptor does insulin upregulate in peripheral tissue?

A

GLUT4

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6
Q

What metabolic changes occur after insulin binds its receptor?

A

(1) ↑ Glycogen
(2) ↑ Anabolism
(3) ↑ TG synthesis

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7
Q

How does insulin decrease serum K+ levels?

A

↑ Activity of Na+/K+ ATPase

(Predominantly in skeletal muscle)

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8
Q

What are the rapid-acting, short-duration insulin analogs?

A

(1) insulin Glulisine
(2) insulin Aspart
(3) insulin Lispro

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9
Q

What insulin analogs are used for control of postprandial glucose spike?

A

(1) insulin Glulisine
(2) insulin Aspart
(3) insulin Lispro

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10
Q

What are the intermediate-acting insulin analogs?

A

(1) Regular insulin
(2) NPH insulin

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11
Q

What is the only insulin analog available for IV administration?

A

Regular insulin

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12
Q

Treatment: Diabetic ketoacidosis

A

IV regular insulin

(Remember to add K+ to avoid hypokalemia)

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13
Q

What hormone can be used to treat hyperkalemia?

A

Insulin

(Remember to add glucose to avoid hypoglycemia)

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14
Q

What are the long-acting insulin analogs?

A

(1) insulin Detemir
(2) insulin Glargine
* (G-_LARGE_-ine is the longest acting insulin analog)*

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15
Q

What is the most common complication of insulin therapy?

A

Hypoglycemia

(Duh!)

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16
Q

MOA: Sulfonylureas

A

Inhibit ATP-dependent K+ channels

  • (↑ Endogenous insulin ∴ ↑ C-peptide)*
  • (↑ Endogenous insulin ∴ Only treats T2DM)*
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17
Q

Suffix: First-generation sulfonylureas

A

“-amide”

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18
Q

Suffix: Second-generation sulfonylureas

A

“-ride”

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19
Q

What second-generation sulfonylurea has the shortest duration of action?

A

Glipizide

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20
Q

Indication: Meglitinides

A

T2DM

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21
Q

Other than hypoglycemia, what is a common side effect of sulfonylureas and meglitinides?

A

Weight gain

22
Q

What class of diabetes drugs can cause a disulfiram-like reaction?

A

First-generation sulfonylureas

23
Q

Suffix: GLP-1 analogs

A

“-tide”

24
Q

What are the physiologic actions of GLP-1?

A

(1) ↓ Glucagon secretion
(2) Delay gastric emptying
* (Satiety, ↓ Glucagon release, Inhibit gastric emptying)*

25
Q

MOA: “-gliptin” drugs

A

Inhibit DDP-4

(And ∴ degradation of GLP-1. Gliptins be GLP-liftin)

26
Q

What class of drugs increases levels of endogenously secreted GLP-1?

A

Gliptins

(Gliptin = GLP-Liftin’)

27
Q

Adverse Effects (2) : DPP-4 inhibitors

A

(1) Nasopharyngitis
(2) URTIs

28
Q

Which diabetes drugs do not cause hypoglycemia?

A

(1) GLP-1 analogs
(2) DDP-4 inhibitors
* (∵ Effects are glucose-dependent, diminishing as glucose levels approach normal)*

29
Q

Can GLP-1 agonists treat T1DM?

A

No

30
Q

Adverse Effect: GLP-1 inhibitors

A

Pancreatitis

31
Q

Name an enzyme that Metformin inhibits and one that it activates

A

(1) Inhibits: mGPD
(2) Activates: AMP Kinase
* (mGPD = Inhibits mitochondrial enzyme glycerophosphate dehydrogenase)*
* (AMPK ↓ Gluconeogenesis and ↑ Insulin sensitivity)*

32
Q

Other than affecting gluconeogenesis, what is the mechanism of Metformin?

A

↑ Insulin sensitivity

(Other aspects include ↓ intestinal absorption of glucose)

33
Q

Adverse Effects (2) : Metformin

A

(1) Lactic acidosis
(2) GI Issues

34
Q

How is Metformin excreted?

A

Renal

(Unaltered and in active form)

35
Q

Name a diabetes drug which may cause weight loss

A

Metformin

36
Q

Suffix: Thiazolidinediones

A

“-glitazone”

37
Q

MOA: Glitazones

A

PPAR-γ ligand

(∴ ↑ Insulin sensitivity and fatty acid oxidation)

38
Q

How do glitazones ↓ serum triglyceride levels?

A

(1) ↑ Fatty acid oxidation
(2) ↑ Differentiation of adipocytes

39
Q

Name 2 proteins that glitazones upregulate

A

(1) Adiponectin
(2) GLUT4

40
Q

Adverse Effects (4) : Glitazones

A

(1) Weight gain
(2) Peripheral edema
(3) ⇒ Heart failure
(4) ↓ Bone mineral density

41
Q

What are the physiologic effects of Amylin?

A

(1) ↓ Gastric emptying
(2) ↓ Glucagon

42
Q

What drug can be used to treat T1DM and T2DM but is not an insulin analog?

A

Amylin

43
Q

Adverse Effects (2) : Amylin

A

(1) Hypoglycemia
(2) GI upset

44
Q

Name 2 α-glucosidase inhibitors

A

(1) Acarbose
(2) Miglitol

45
Q

What is the mechanism of α-glucosidase inhibitors in treating diabetes?

A

↓ Intestinal glucose absorption

46
Q

Why are α-glucosidase inhibitors infrequently prescribed?

A

Severe abdominal side effects

(Undigested GI sugars ∝ Symptoms of lactose intolerance)

47
Q

Suffix: SGLT2 inhibitors

A

“-flozin”

48
Q

MOA: “-flozin” drugs

A

Inhibit SGLT2

(In proximal convoluted tubule ∵ that’s where everything is reabsorbed)

49
Q

Adverse Effects (3) : SGLT2 inhibitors

A

(1) ↑ Frequency of urination
(2) UTIs
(3) ↑ Risk of vaginal candidiasis

(↑ Urination ⇒ Hypotension)

50
Q

Contraindication: SGLT2 inhibitors

A

Renal sufficiency

3b_Boards - SketchyPharm (32 decks)

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