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Pharm Exam 6 > L 33-34 Diabetes > Flashcards

L 33-34 Diabetes Flashcards

1
Q

Insulin lispro (Humalog)

A

Rapid acting insulin

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2
Q

Insulin aspart (NovoLog)

A

Rapid acting insulin

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3
Q

Insulin glulisine (apidra)

A

Rapid acting insulin

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4
Q

Regular insulin (Novoline R, Humulin R)

A

Regular or short acting insulin

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5
Q

NPH or Isophane Insulin (Humulin N, Novolin N)

A

Intermediate acting insulin

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6
Q

Insuline glargine (Lantus)

A

Long acting insulin

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7
Q

Insulin detemir (Levemir)

A

Long acting insulin

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8
Q

Insulin degludec (Tresiba)

A

Long acting insulin

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9
Q

How is insulin released from the beta cells in the pancreas?

A

Anything that increases energy in the beta cells will increase the release of insulin. This is primarily glucose, which is taken up by GLUT-2 transporters leading to an increase in ATP. Increased ATP causes closing of K channels in the membrane leading to depolarization. Depolarization causes Ca channel opening which signals exocytosis of stored insulin.

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10
Q

What increases release of insulin vs that which decreases release?

A

Increased Release: glucose, sugars, amino acids, fatty acids, ketone bodies, beta-2 agonists, vagal stimulation
(note that beta-2 stimulation increases insulin release and therefore beta blockers will inhibit release and cause hyperglycemia

Decreased Release: alpha-2 agonists, conditions activation sympathetic stimulation like hypoxia, hypothermia, surgery, burns)

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11
Q

What are the insulin dependent and independent tissues?

A

Dependent: muscle, fat, heart, leukocytes

Independent: brain, RBC’s, liver

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12
Q

What are the effects on the body when insulin is injected?

A

Blood glucose will decrease
Blood pyruvate and lactate will increase because of the increased glucose metabolism
Inorganic phosphates will decrease because they are being used to make glycogen
Plasma potassium decreases–important to remember that this can kill a patient already hypokalemic

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13
Q

Where are GLUT-1 transporters found and how do they function?

A

GLUT-1 transporters are found in all tissues, but especially in RBC’s and the brain. They are responsible for basal uptake of glucose and transport across the BBB. Km=1-2mmol/L

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14
Q

Where are GLUT-2 transporters found and how do they function?

A

Found in beta cells of the pancreas, liver, kidney, gut
Important in the regulation of insulin release
Km=15-20 mmol/L

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15
Q

Where are GLUT-3 transporters found and how do they function?

A

Found in the brain, kidney, placenta, other tissues
Km less than 1
Used for glucose uptake into neurons and other tissues

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16
Q

Where are GLUT-4 transporters found and how do they function?

A

Found in muscle, heart, adipose, and other
Km=5 mmol/L
Insulin mediated function

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17
Q

Where are GLUT-5 transporters found and how do they function?

A

Found in the gut and kidney
Km= 1-2 mmol/L
Used in the absorption of fructose

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18
Q

How is insulin metabolized?

A

Insulin is cleared from the body by the liver and the kidneys which break the disulfide bond between the A and B chains

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19
Q

What are symptoms of hypoglycemia?

A

Tachycardia–from the catecholamines being released to counter the low blood sugar
Confusion–from low glucose to the brain
Vertigo–
Diaphoresis–

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20
Q

What happens if insulin is injected repeatedly in the same location?

A

lipodystrophy and lipohypertrophy can occur because insulin is anabolic for adipose tissue

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21
Q

Which insulins have been approved for use in IVs?

A

Only the rapid and short acting insulins can be used in IV

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22
Q

When is Glucagon not effective in increasing blood glucose levels?

A

Juveniles don’t respond as well as adults

Anyone with poorly controlled diabetes or low stores of glycogen will not respond well to glucagon

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23
Q

What other effects does glucagon have on the body besides glycogen breakdown?

A

Potent inotropic and chronotropic agent in the heart–can be used to overcome beta blocker toxicity

Produces profound relaxation of the intestines

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24
Q

Diazoxide (Proglycem)

A

Non-Diuretic thiazide, vasodilator, hyperglycemic
Mechanism: blocks the ATP-dependent K+ channel and thereby inhibits the release of insulin
Use: patients with insulinoma
Administered orally

Adverse: overdose causes hyperglycemia with ketoacidosis, hypotension from small diuretic effect of losing Na+ and water, excessive hair growth–especially in kids

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25
Q

How do sulfonylurea drugs work?

A

Block the K+ channel in beta cells which depolarizes the cell and Ca++ influx and thereby the release of insulin
Add photo slide 30

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26
Q

Adverse effects of sulfonylurea drugs

A

Hypoglycemia: from producing too much insulin for the need, worse with longer acting drugs
Weight gain: from the anabolic effects of insulin on adipose tissue
Sulfa allergic reaction

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27
Q

Tolbutamide

A

First generation sulfonylurea and therefore no longer prescribed
This was the best of the first gen. drugs because of a short half-life of 4-5 hours which allowed infrequent episodes of hypoglycemia and made it safe for the elderly

28
Q

Chlorpropamide

A

First generation sulfonylurea and therefore no longer prescribed
Half-life of 32 hours making it the worst as far as hypoglycemic effects

29
Q

Tolazamide

A

First gen. sulfonylurea and no longer used

30
Q

Glyburide

A

Second generation sulfonylurea

24 hour effect making it the worst for hypoglycemia

31
Q

Glipizide

A

2nd generation sulfonylurea

Short half-life of 2-4 hours making it the best (least) hypoglycemic of 2nd gen. drugs

32
Q

Glimepiride

A

2nd generation sulfonylurea
Once-a-day dosing
Has little hypoglycemic effect

33
Q

Meglitinide drug class

A

Same mechanism of action as sulfonylureas but without being sulfa derivatives–good for having the same effects but for people with sulfa allergies
Rapid and short acting–mimics insulin better than sulfonylureas
Less hypoglycemia than sulfonylureas, and little effect on weight gain
Downside is they are administered orally 10 min before meals

34
Q

Repaglinide (Prandin)

A 
Meglitinide class of drug
Blocks the ATP-dependent K+ channel in beta cells leading to insulin release
35
Q

Nateglinide (Starlix)

A 
Meglitinide class of drug
Blocks the ATP-dependent K+ channel in beta cells leading to insulin release
36
Q

Metformin (Glucophage)

A

Decreases blood glucose without releasing insulin
Mechanism: increases glucose uptake, decreases glucose absorption from GI, dec glucagon, dec gluconeogenesis

DOC for DM II because does not increase body weight like sulfonyureas, decreases macrovascular events, safe for kids older than 10

Administered orally

Adverse: Lactic acidosis (can cause death) and diarrhea (top 5 worst drugs for diarrhea)

Contraindications: Renal disease, liver disease, alcoholism, anything leading to hypoxia like CHF, COPD, etc.
These affect the Cori or Lactic acid cycle causing an increase in lactic acid
Photo from slide 37

37
Q

Thiazolidinediones (-glitazones, TCDs)

A

These are insulin sensitizers targeting insulin resistance.
Binds nuclear receptor PPAR-gamma which can cause post-receptor insulin-mimetic action like increasing the number of GLUT-4 receptors available
Long half-life makes for long onset and offset of effects

Therapeutics: lowers insulin resistance, lowers triglycerides in long-term, can be used prophylactically for DM II

Orally, metabolized by liver

Adverse: Edema and weight gain

Contraindications: Do not use in patients with hepatic disease or CHF

38
Q

Pioglitazone (Actos)

A

Insulin sensitizer in the Thiazolidinedione class

39
Q

Rosiglitazone (Avandia)

A 
Insulin sensitizer in the Thiazolidinedione class
May have more side-effects than Pioglitazone
40
Q

Alpha-glucosidase inhibitor drug class

A

Reduces glucose absorption by inhibiting the enzyme needed to breakdown complex carbs into simpler carbs that can be absorbed
Mild drugs will little effect on diabetes or weight gain

Administered orally

Frequent GI effects from the increased sugars available to the gut bacteria–diarrhea and flatulence

41
Q

Acarbose (Precose)

A

Alpha-glucosidase inhibitor that inhibits uptake of glucose from the small intestines and thereby decreases sugars available to the body.

42
Q

Miglitol (Glyset)

A

Alpha-glucosidase inhibitor that inhibits uptake of glucose from the small intestines and thereby decreases sugars available to the body.

43
Q

Why is there a difference in insulin level response between orally and IV administered glucose?

A

Orally administered glucose activates incretins which induce insulin secretion from beta cells and inhibits glucagon release from alpha cells

44
Q

Incretin Mimetic drug class

A

Synthetic versions of endogenous incretins used to stimulate the pancreas to produce more insulin and less glucagon
All injected, either once daily or weekly
Have potential to increase beta cell number and function
Slow gastric emptying
Promotes weight loss!
Adverse: GI disturbance, hypoglycemia if combined with other therapies, acute pancreatitis!
Contraindications: slow GI, renal impairment, Liraglutide may cause thyroid cancer

45
Q

Exenatide (Byetta)

A

Incretin mimetic
Increases insulin release and decreases glucagon release
Injected once weekly

46
Q

Liraglutide (Victoza)

A

Incretin mimetic
Increases insulin release and decreases glucagon release
May cause thyroid cancer (shown in animals only at this point)
Injected once daily

47
Q

Dulaglutide (Trulicity)

A

Incretin mimetic
Increases insulin release and decreases glucagon release
Injected once weekly

48
Q

DPP-IV inhibitor drug class (gliptins)

A

These drugs inhibit DPP-IV enzyme which usually breaks down endogenous incretins. Inhibiting this enzyme allows stimulation of the pancreas to produce more insulin and less glucagon
Has no effect on weight
Administered orally (often preferred over other incretin mimetic drugs)
Adverse: acute pancreatitis and pancreatic cancer
Contraindicated in slow GI problems and renal impairment

49
Q

Sitagliptin (Januvia)

A

DPP-IV inhibitor

Extends life and effects of endogenous incretins

50
Q

Saxagliptin (Onglyza)

A

DPP-IV inhibitor

Extends life and effects of endogenous incretins

51
Q

Linagliptin (Tradjenta)

A

DPP-IV inhibitor

Extends life and effects of endogenous incretins

52
Q

Alogliptin (Nesina)

A

DPP-IV inhibitor

Extends life and effects of endogenous incretins

53
Q

Pramlintide (Symlin)

A

Amylin-like peptide drug class
Must be used with insulin
Only insulin adjunct therapy approved for use in type I and II DM
Works by regulating post-prandial blood glucose by: decreasing gastric emptying, suppressing glucagon secretion, centrally regulating appetite
Causes weight loss
Requires 3 injections/day

54
Q

Bromocriptine (Cycloset)

A

Dopamine agonist used to prevent the sympathetic spike in the morning that would stimulate the liver to produce glucose and put out fats for energy use.
Used to decrease blood glucose and fat levels
Weight neutral
Reduces CV problems in diabetics
Must be taken orally within 2 hours of awakening

55
Q

Colesevelam (WelChol)

A

Bile acid binding resin
Mechanism unknown
Decreases plasma glucose and lipids
Causes constipation and bloating (perhaps because not absorbed and stays in GI)

56
Q

SGLT2 inhibitor drug class

A

Newest class
Mechanism: Inhibits the Na+/glucose co-transporter in the kidney so patients pee out their glucose
Given orally
Adverse: female mycotic infections, UTIs, increased urinary frequency, osmotic diuresis causing postural dizziness, orthostatic hypotension, syncope, dehydration; causes renal problems, increased LDL
Not used in patients with renal impairment or if prone to UTI’s

57
Q

Canagliflozin (Invokana)

A

SGLT2 inhibitor

58
Q

Dapagliflozin (Farxiga)

A

SGLT2 inhibitor

59
Q

Empagliflozin (Jardiance)

A

SGLT2 inhibitor

60
Q

What drug class is known for causing lactic acidosis?

A

Metformin

61
Q

Which drug classes decrease weight?

A

Incretin Mimetics

Pramlintide

62
Q

Which drug classes have problems with hypoglycemia and hyperinsulinemia?

A

Sulfonylureas

Meglitinides

63
Q

Which drug classes are injected?

A

Incretin mimetics
Pramlintide
(these are also the drugs that cause weight loss)

64
Q

Which drug classes cause the least GI symptoms?

A

Thiazolidinediones

Gliptins

65
Q

Which drug can also help lower LDL levels?

A

Metformin

66
Q

Which drug classes cause weight gain?

A

Sulfonylureas

Thiazolidinediones

Pharm Exam 6 (10 decks)

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