Diabetes Flashcards

1
Q

What is the pathology of type 1 DM?

A

Autoimmune destruction of beta cells in the pancreas. Patients have little to no insulin

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2
Q

What is the pathology of type 2 DM?

A

Increased resistance to insulin. Patients have normal or elevated insulin

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3
Q

Which DM (type 1 or 2) is associated with juvenile onset?

A

Type 1; remember, type 2 is a later onset (familial, assc with obesity)

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4
Q

Which DM (type 1 or 2) absolutely requires exogenous insulin as a treatment?

A

Type 1

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5
Q

What glucose receptor is on the pancreatic beta cells?

A

GLUT 2

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6
Q

What glucose receptor is on muscle/adipose tissue?

A

GLUT 4

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7
Q

Describe a glucose tolerance test

A

Check the patient’s blood levels of glucose and insulin. Then, give the patient oral glucose. Then check their blood glucose measure BG and insulin again. Obviously in a diabetic, the BG will be elevated

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8
Q

Insulin is secreted as proinsulin, a single chain made of 3 components (alpha chain, beta chain, and C peptide). Which 2 of these are joined by disulfide bonds?

A

The alpha and beta chains

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9
Q

Insulin is secreted as proinsulin, a single chain made of 3 components (alpha chain, beta chain, and C peptide). Which of these components is measured in the blood as a marker of endogenous insulin production?

A

C peptide

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10
Q

Physiology review: List the steps in insulin secretion starting with GLUT 2 uptake of circulating glucose

A
  1. Glucose is elevated so GLUT 2 takes in circulating glucose (into pancreatic beta cell)
  2. Glucose is generated to ATP
  3. ATP closes the K channel of beta cell
  4. Cell is depolarized
  5. Depolarization –> influx of Calcium
  6. Influx of Ca causes exocytosis of insulin granules into blood
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11
Q

What do alpha cells of the islets of langerhans make?

A

Glucagon

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12
Q

What do beta cells of the islets of langerhans make?

A

Insulin

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13
Q

What do delta cells of the islets of langerhans make?

A

Somatostatin

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14
Q

What are 4 stimulants of insulin release?

A
  1. Increased blood glucose
  2. Increased blood amino acids
  3. Vagal stimulation
  4. Increased sulfonyl ureas
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15
Q

What are 2 amplifiers of insulin release?

A
  1. Enteric hormones: gastrin, cholecystokinin (CCK), and secretin
  2. Beta adrenergic stimulation
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16
Q

What are 3 inhibitors of insulin release?

A
  1. Somatostatin
  2. Drugs (such as diazoxide)
  3. Catecholamines (Epi, Norepi)
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17
Q

Describe a ketoacidotic coma

A

Caused by low insulin –> increased liver ketone production (beta-hydroxybutyrate & acetoacetate) –> decreased pH, fruity breath odor, Kussmaul breathing, hyperglycemia

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18
Q

How do you treat a ketoacidotic coma (diabetic ketoacidosis)?

A

Give insulin (also IV fluids if they are dehydrated)

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19
Q

Diabetic ketoacidosis is usually seen in type 1 or 2 DM?

A

Type 1

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20
Q

Describe a hypoglycemic coma

A

Caused by insulin overdose. It is so common that all comatose patients are given glucose while you wait for labs

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21
Q

Tx of hypoglycemic coma?

A

Glucose.. duh

22
Q

Hypoglycemic coma is usually in type 1 or 2 DM?

A

Type 2

23
Q

This is a blood test for long term BG control

A

HbA1C

24
Q

The 3 principal types of insulin secretion are?

A
  1. Short acting/ short half life
  2. Intermediate acting/ longer half life
  3. Long acting/ longest half life (largest crystals)
25
Q

Short acting insulin is called “Regular insulin”. what is unique about it?

A

Is is the only form that can be injected IV. All others are IM or SC

26
Q

NHP preps are short, intermediate, or long acting?

A

Intermediate

27
Q

Lente insulins are short, intermediate, or long acting?

A

Intermediate, they are 30% short acting and 70% ultralenta (long acting)

28
Q

These forms of insulin alter the isoelectric point of insulin to drastically increase half life and thus are very long acting

A
  1. Insulin glargine

2. Insulin demetir

29
Q

How is insulin glargine formed?

A

Switch the B21 asparagine to glycine and add 2 asparagines to B-chain C terminus

30
Q

These drugs are benzoic acid derivatives that increase insulin secretion. They have rapid GI absorption

A

The Meglitinides: Repaglinide, Nateglinide
**Increased insulin secretion via blocking potassium channels in pancreatic beta cells –> depolarization –> Ca influx –> insulin secretion

31
Q

How does insulin demetir work?

A

It is acidic, so when it is injected it neutralizes and forms a precipitate

32
Q

How does Metformin & Phenformin work (the biguanides)?

**Phenformin was withdrawn due to lactic acidosis AE

A

Decrease hepatic gluconeogenesis. Also decreases GI glucose absorption & increases peripheral tissue insulin sensitivity (according to Medscape)

33
Q

Name the sulfonylureas (4)

A
  1. Glyburide
  2. Glipizide
  3. Gliclazide
  4. Glimepiride
34
Q

Does metformin affect insulin secretion?

A

No! This is a good thing bc it means that metformin has no hypoglycemia AE
Medscape: Metformin has BBW of Lactic acidosis

35
Q

What is the MOA, metabolism, & elimination of the sulfonylureas?

A

MOA: increase insulin sensitivity in peripheral tissues
Metabolism: hepatic
Elimination: renal

36
Q

What drug class enhances the hypoglycemic action of sulfonylureas?

A

NSAIDs

37
Q

What the alpha-glucosidase inhibitors and how do they work?

A

Acarbose: reduce intestinal absorption of starch, disaccharides by inhibiting brush border alpha-glucosidase. They reduce post-prandial BG elevation. **Are not used alone

38
Q

What is the absorption, metabolism, and AE of the Meglitinides?

A

Absorption: GI (rapid)
Metabolism: Hepatic
AE: Hypoglycemia

39
Q

What is the dipeptidyl peptidase-4 inhibitors & how do they work?

A

Sitagliptin- inhibits dipeptidyl peptidase-4 which acts to degrade incretin hormones

40
Q

When are the meglitinides taken?

A

Before a meal (to control post-prandial BG)

41
Q

What is the absorption and metabolism of metformin

A

Oral absorption, no metabolism

42
Q

How does Rosiglitazone & Pioglitazone (the Thiazolidinediones) work?

A

Bind to PPAR-gamma. Major drug for increasing insulin sensitivity in peripheral tissues by increasing GLUT-4 activity

43
Q

What is the absorption & metabolism of Rosiglitazone & Pioglitazone?

A

Oral absorption, little metabolism

44
Q

What is the somatostatin analog & how does it work?

A

Ocreotide: works like somatostatin –> inhibits insulin/glucagon secretion from pancreas. **Useful for tx of insulinomas/glucagonomas
**Also could treat GH adenoma bc somatostatin inhibits GH!

45
Q

What is the bile acid sequestrate?

A

Colesevelam hydrochloride

46
Q

How does Colesevelam hydrochloride work?

A

Lowers blood cholesterol and lowers HbA1C- so treats DM & high cholesterol (thats a start for metabolic syndrome**)

47
Q

MOA of Colesevelam hydrochloride?

A

Interrupts enterohepatic cycling, lowers farsenoid X receptor activation

48
Q

AE of Colesevelam?

A

GI

49
Q

Cinagliflozin MOA

A

SGLT-2 inhibitor; SGLT-2 is a Na-glucose transporter in kidney responsible for 90% of reabsorption of glucose (inhibiting the transporter would cause increased urine glucose)

50
Q

AE’s of Cinagliflozin?

A

Hypotension, Hyperkalemia, decreased BG, increased LDL; contra w/ renal dz & dialysis