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Adv Pharm 1 > Endo (pt 6/7) Pancreas > Flashcards

Endo (pt 6/7) Pancreas Flashcards

1
Q

The Hormone containing cells of the pancreas

A

Islets of Langerhan

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2
Q

What are the secretory products of the Beta Cell?

A

-Insulin
-C-peptide
-Proinsulin
-Amylin

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3
Q

Storage & anabolic hormone of the body

A

Insulin

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4
Q

Modulates appetite, gastric emptying, glucagon & insulin secretion

A

Islet amyliod polypeptide (IAPP, amylin)

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5
Q

Hyperglycemic factor that mobilizes glycogen stores (glucose back into the system)

A

Glucagon (opposite of insulin)

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6
Q

Universal inhibitor of secretory cells

A

Somatostatin

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7
Q

Small protein that facilitates digestive processes

A

Pancreatic Peptide

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8
Q

Peptide that increases GH release

A

Ghrelin

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9
Q

Insulin dependent diabetes – selective beta cell destruction & severe or absolute insulin deficiency
-Autoimmune or Idiopathic

A

Type 1

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10
Q

Non-Insulin dependent diabetes – tissue resistance to the action of insulin combined with a relative deficiency in insulin secretion
-Results in increase in obesity

A

Type 2

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11
Q

Other specific causes of an elevated blood glucose:
-pancreatectomy
-pancreatitis
-nonpancreatic diseases
-drug therapy (i.e. corticosteroid therapy)

A

Type 3

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12
Q

Gestational Diabetes (GDM) – placenta & placental hormones create an insulin resistance
-Typically 3rd trimester

A

Type 4

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13
Q

Explain the physiology behind the release of insulin.

A

1) Glucose enters the cell via glucose transporter
2) Glucose metabolism signals ATP production to increase
3) ATP production signals K+ channel to stop allowing the efflux of K+
4) K+ levels rise, depolarizing the beta cell
5) Depolarization allows Calcium to enter the cell, allowing for the exocytosis of Insulin

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14
Q

What factors increase insulin release?

A

-Glucose
-some hormones
-Beta SNS activity
-High concentrations of fatty acids
-Glucagon
-Cholecystokinin

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15
Q

What factors decrease insulin release?

A

-Insulin
-Leptin
-Amylin
-Somatostatin
-Alpha SNS activity
-Chronic increased glucose
-Low concentration of fatty acids.

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16
Q

What is the MOA of insulin?

A

Binds to the Insulin Receptor on the membrane of most tissues

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17
Q

What are the effects of Insulin binding to its receptor?

A

-↑ glucose uptake
-↑ glycogen synthase activity (enzyme needed for glycogenesis)
-↑ glycogen formation
-Effects on protein synthesis, lipolysis and lipogenesis
-Enhancement of DNA synthesis

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18
Q

T/F: Glucose decreases the affinity of the insulin receptor for insulin.

A

True

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19
Q

Endogenous insulin is 60% cleared by the _____, and the remaining by the _____.

A

60% in Liver, remaining 35-40% in Kidney

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20
Q

Exogenous insulin is 60% cleared by the _____, and the remaining by the _______.

A

60% in Kidney; remaining in Liver

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21
Q

What can stimulate the release of Insulin?

A

-Increased BG
-Incretins (metabolic hormones that cause a dec in BG levels)
-Vagal nerve stimulation

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22
Q

T/F: Insulin promotes the synthesis and storage of glycogen, triglycerides, and protein in its major target tissues: liver, fat, and muscle.

A

True

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23
Q

-Fast onset and short duration (<4-5 hrs)
-Permit more physiologic prandial insulin replacement

A

Rapid-Acting Insulin (Lispro, Aspart, Glulisine)

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24
Q

-Rapid Onset (30 min)
-Peaks at 2-3 hrs
-Duration of action: 5-8 hrs

A

Short-acting (regular) Insulin

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25
Q

-Onset = 2-5 hrs
-DOA = 4-12 hrs

A

Intermediate Acting Insulin (NPH)

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26
Q

-Onset = 1-2 hrs
-DOA = 11-24 hrs

A

Long-acting (Glargine, Detemir)

Note: Detemir allows a smooth background insulin level with BID dosing - DOA = 12 hrs

27
Q

What is the tx for DKA? (breakdown of fats/ketones = toxic levels of ketoacids)

A

Regular Human insulin @ 0.1 IU/kg/hr IV

28
Q

-Profound hyperglycemia and dehydration seen in Type 2 DM
-Seen especially in the elderly (Inadequate oral hydration)
-Tx: Low-dose insulin (regular) and titrate to effect

A

Hyperosmolar Hyperglycemic Syndrome

29
Q

What is the preferred treatment for the abrupt onset of hyperglycemia or the appearance of ketoacidosis in the periop period?

A

Regular Insulin
-IV or SQ
-1-5 U IV or 0.5-2 U/h IV insulin (Insulin calculator)
-Trigger is BG > 200 intra-op

30
Q

What is the most common complication of insulin therapy?

A

Hypoglycemia

31
Q

What are other complications of insulin therapy?

A

-Immunopathology (antibodies, allergy, immune resistance)
-Lipodystrophy at injection site (r/t animal prepartions - atrophy of sq tissues)
-Drug interactions
-Increased risk of cancer

32
Q

What is immune insulin resistance?

A

A low titer of circulating IgG anti-insulin antibodies that neutralize the action of insulin.

33
Q

What are some drugs that interact with insulin?

A

ACTH, estrogens, glucagon, epinephrine guanethidine, certain antibiotics, salicylates, phenylbutazone, MAOI

34
Q

What are the 6 MOAs of Oral anti-diabetic agents?

A
  1. Bind to Sulfonylurea receptor and stimulate insulin secretion
  2. Lower glucose levels by their actions on liver, muscle and adipose
  3. Slow the intestinal absorption of glucose
  4. Mimic incretin effect or prolong incretin action
  5. Inhibit the reabsorption of glucose in the kidneys
  6. Not really sure…ill-define mechanisms
35
Q

What is the mechanism of action of the Sulfonylureas?

A

Bind to the sulfonylurea receptor, inhibiting the efflux of K+, causing depolarization of the cell, Voltage-Gated Ca channels to open, and insulin to be released.

36
Q

What is the difference between the 1st and 2nd generation of sulfonylureas?

A

2nd gen is 100-200x more potent than 1st.
-Decreased adverse effects
-Decreased drug interactions

37
Q

What are the 1st generation sulfonylureas?

A

-Tolbutamide (safest for elderly diabetics)
-Chlorpropamide
-Tolazamide

38
Q

What are the 2nd generation sulfonylureas?

A

Prescribed more frequently due to decreased adverse effects and drug interactions.
-Glyburide
-Glipizide (shortest 1/2 life)
-Glimepiride (once daily, low dosing. Can be used as a monotherapy or in combo with insulin)

39
Q

What is the metabolism of the 1st and 2nd generation of sulfonylureas?

A

Hepatic

40
Q

What populations should you caution the use of sulfonylureas in?

A

-CAD or CV Issues
-Elderly
Anyone who, if they got hypoglycemic, it’d be bad.

41
Q

Drug that modulates beta cell insulin release by regulating K+ efflux.
-Fast onset
-DOA 4-7 days
-Hepatically cleared by CYP3A4 (!!)
-hypoglycemia is a risk if meal is delayed, skipped, or lacks carbs
-Ok for use in renal patients and elderly
-Does not contain sulfur (good for sulfur allergies)
-Monotherapy or with Biguanides

A

Repaglinidine (Meglitinide Analogs)

42
Q

A drug that stimulates very rapid & transient release of insulin from beta cells through closure of the ATP-sensitive K+ channel.
-Hepatically cleared by CYP2C9 and CYP3A4
-Monotherapy or with Biguanides
-OK for use in renal patients and elderly
-Lowest incidence of all the secretagogues of hypoglycemia

A

Nateglinide (D-phenylalanine Derivative)

43
Q

What is the MOA of the Biguanides (Metformin)?

A

Reduces hepatic glucose production through activation of the enzyme AMP-activated protein kinase (AMPK)

44
Q

Why is Metform called a euglycemic agent?

A

Because patients taking Biguangides experience less fasting as well as post prandial hyperglycemia and hypoglycemia is also rare.
-Avoids hyperglycemia with fasting and avoid hypoglycemia with therapy. Good at maintaining euglycemia.

45
Q

How is Metformin metabolized?

A

Not metabolized at all, excreted by the kidneys as an active compound. Concern in patients with liver/kidney issues.

46
Q

How can Metformin cause Lactic Acidosis?

A

If patient has renal insufficiency, drug levels buildup and can block gluconeogenesis and higher risk of lactic acidosis damaging liver.
-Concern in patients with liver/kidney issues.
-Can impair the liver’s metabolism of lactic acid (lactic acidosis).

47
Q

What are contraindications to the use of Metformin?

A

R/t risk of Lactic Acidosis:
-Renal Dz
-Alcoholism
-Hepatic Dz
-Conditions with a predisposition to tissue anoxia

48
Q

What are toxicity symptoms of Metformin?

A

-GI (anorexia/N/V/D/abd pain) - 20% of patients. Transient and dose related, but persistent diarrhea causes D/C in 3-5% of patients
-Vit B12 deficiency
-Lactic acidosis – therapy should be held on the day of IV contrasted studies due to renal stress

49
Q

What is the MOA of the Thiazolidinediones (Tzds)

A

-Act to decrease insulin resistance
-ligands of peroxisome proliferator-activated receptor-gamma (PPAR-γ)
-Increase glucose transporter expression
-Decrease free fatty acid levels
-Decrease hepatic glucose output

50
Q

PPAR-y receptors modulate the expression of genes involved in:

A

-Lipid & glucose metabolism
-Insulin signal transduction
-Adipocyte and other tissue differentiation

51
Q

What is the MOA of Rosiglitazone (Avandia) - A Thiazolidinedione (Tzds)

A

-Regulates gene expression by binding to PPAR-Y
-Reduces insulin resistance
-long-acting oral agent, rapidly absorbed and highly protein bound
-Hepatic metabolism (CYP2C8) to minimally active metabolites

52
Q

What are the toxicity symptoms of the Thiazolidinediones (Rosiglitazone and Pioglitazone)? (!!!!!)

A

-Fluid retention
-Edema
-Weight Gain
-Anemia
-Bone Fx in women

Cannot use in CHF or Hepatic Dz, may worsen heart disease (really bad in Rosiglitazone (Avandia) ).

53
Q

What is the MOA of Pioglitazone (Actos) - A Thiazolidinedione (Tzds)?

A

-Regulates gene expression by binding to PPAR-γ and PPAR-α (!)
-Reduces insulin resistance (Type 2 DM)
-Long-acting oral agent (>24h)
-Hepatic metabolism (CYP2C8 & CYP3A4) to active metabolites

54
Q

What are the examples of the Alpha-Glucosidase Inhibitors (slow the intestinal absorption of glucose)?

A

Acarbose & Miglitol

55
Q

What is the MOA of Acarbose & Miglitol?

A

-Competitive inhibitors of the intestinal α-glucosidases
-Reduce post-meal excursions by delaying the digestion & absorption of starch & disaccharides
-Not metabolized
-Renally excreted – not for renal failure patients

Decreases fasting glucose levels
-Blocks sucrose > glucose
-Inhibits glucoamylase, alpha amylase, and sucrase.

Rarely used in the US

56
Q

Hypoglycemia associated with Acarbose & Miglitol (Alpha-Glucosidase Inhibitors) must be treated with what?

A

Glucose; the metabolism of sucrose is blocked

57
Q

What is the MOA of Colesevelam Hydrochloride?

A

-Developed as a bile acid sequestrant and cholesterol lowering drug
-Approved as a DMII antihyperglycemic therapy
-Unknown MOA
-Not systemically absorbed
-Side effects: GI complaints

58
Q

What is the MOA of Pramlintide?

A

-Synthetic analog of Amylin
-Injectable (used in combo with OHAs)
-Pre-prandial use in DM1 and 2 for modulation of post-prandial glucose levels
-Suppresses glucagon release, delays gastric emptying, and has CNS-mediated anorexic effects
-Renal metabolism and excretion
-Major adverse effects: Hypoglycemia & GI symptoms (N/V and anorexia)

59
Q

Where is glucagon synthesized?

A

Synthesized in alpha cells of the pancreatic islets of Langerhans.

60
Q

A Catabolic hormone that acts to mobilize glucose, fatty acids, and amino acids into the systemic circulation.
-Degraded by the liver, kidney, plasma, and tissue receptor sites

A

Glucagon

61
Q

What are the pharmacologic effects of Glucagon?

A

Increases cAMP, breaking down (catabolism) of stored glycogen, and increasing gluconeogenesis and ketogenesis.
-Potent inotropic and chronotropic effects on the heart

62
Q

What are the clinical uses of Glucagon?

A

-Severe hypoglycemia
-BB overdoses (Increases cAMP on heart without activating Beta receptors
-Diagnosis of Endocrine Disorders
-Radiology of the bowel (relaxes the bowel, but be careful not to push it too quickly as it produces N/V) (!!!)

63
Q

When is glucagon contraindicated?

A

In Pheochromocytoma (glucagon promotes catechol release from the Pheo - bad).

Adv Pharm 1 (28 decks)

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