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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
How do sulfonylurea drugs work?
Block the K+ channel in beta cells which depolarizes the cell and Ca++ influx and thereby the release of insulin Add photo slide 30
26
Adverse effects of sulfonylurea drugs
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
27
Tolbutamide
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
Chlorpropamide
First generation sulfonylurea and therefore no longer prescribed Half-life of 32 hours making it the worst as far as hypoglycemic effects
29
Tolazamide
First gen. sulfonylurea and no longer used
30
Glyburide
Second generation sulfonylurea | 24 hour effect making it the worst for hypoglycemia
31
Glipizide
2nd generation sulfonylurea | Short half-life of 2-4 hours making it the best (least) hypoglycemic of 2nd gen. drugs
32
Glimepiride
2nd generation sulfonylurea Once-a-day dosing Has little hypoglycemic effect
33
Meglitinide drug class
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
Repaglinide (Prandin)
``` Meglitinide class of drug Blocks the ATP-dependent K+ channel in beta cells leading to insulin release ```
35
Nateglinide (Starlix)
``` Meglitinide class of drug Blocks the ATP-dependent K+ channel in beta cells leading to insulin release ```
36
Metformin (Glucophage)
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
Thiazolidinediones (-glitazones, TCDs)
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
Pioglitazone (Actos)
Insulin sensitizer in the Thiazolidinedione class
39
Rosiglitazone (Avandia)
``` Insulin sensitizer in the Thiazolidinedione class May have more side-effects than Pioglitazone ```
40
Alpha-glucosidase inhibitor drug class
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
Acarbose (Precose)
Alpha-glucosidase inhibitor that inhibits uptake of glucose from the small intestines and thereby decreases sugars available to the body.
42
Miglitol (Glyset)
Alpha-glucosidase inhibitor that inhibits uptake of glucose from the small intestines and thereby decreases sugars available to the body.
43
Why is there a difference in insulin level response between orally and IV administered glucose?
Orally administered glucose activates incretins which induce insulin secretion from beta cells and inhibits glucagon release from alpha cells
44
Incretin Mimetic drug class
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
Exenatide (Byetta)
Incretin mimetic Increases insulin release and decreases glucagon release Injected once weekly
46
Liraglutide (Victoza)
Incretin mimetic Increases insulin release and decreases glucagon release May cause thyroid cancer (shown in animals only at this point) Injected once daily
47
Dulaglutide (Trulicity)
Incretin mimetic Increases insulin release and decreases glucagon release Injected once weekly
48
DPP-IV inhibitor drug class (gliptins)
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
Sitagliptin (Januvia)
DPP-IV inhibitor | Extends life and effects of endogenous incretins
50
Saxagliptin (Onglyza)
DPP-IV inhibitor | Extends life and effects of endogenous incretins
51
Linagliptin (Tradjenta)
DPP-IV inhibitor | Extends life and effects of endogenous incretins
52
Alogliptin (Nesina)
DPP-IV inhibitor | Extends life and effects of endogenous incretins
53
Pramlintide (Symlin)
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
Bromocriptine (Cycloset)
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
Colesevelam (WelChol)
Bile acid binding resin Mechanism unknown Decreases plasma glucose and lipids Causes constipation and bloating (perhaps because not absorbed and stays in GI)
56
SGLT2 inhibitor drug class
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
Canagliflozin (Invokana)
SGLT2 inhibitor
58
Dapagliflozin (Farxiga)
SGLT2 inhibitor
59
Empagliflozin (Jardiance)
SGLT2 inhibitor
60
What drug class is known for causing lactic acidosis?
Metformin
61
Which drug classes decrease weight?
Incretin Mimetics | Pramlintide
62
Which drug classes have problems with hypoglycemia and hyperinsulinemia?
Sulfonylureas | Meglitinides
63
Which drug classes are injected?
Incretin mimetics Pramlintide (these are also the drugs that cause weight loss)
64
Which drug classes cause the least GI symptoms?
Thiazolidinediones | Gliptins
65
Which drug can also help lower LDL levels?
Metformin
66
Which drug classes cause weight gain?
Sulfonylureas | Thiazolidinediones

Pharm Exam 6 (10 decks)

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