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Endocrine 2 > Diabetes Pharm > Flashcards

Diabetes Pharm Flashcards

1
Q

Rapid acting insulins

A
  • Aspart
  • Lispro
  • Glulisine
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2
Q

Short acting insulin

A

Regular insulin

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3
Q

Intermediate acting insulin

A

-NPH-neutral protamine Hagerdorn

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4
Q

Long acting Insulin

A
  • Detemir

- Glargine

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5
Q

what is the Amylin analog

A

Pramlintide

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6
Q

What are the categories of insulin secretagogues?

A
  • Incretin mimetics: GLP-1 agonist and Dipeptidyl Peptidase-4 (DDP-4) inhibitors
  • K-ATP channel blockers: Sulfonylureas and Meglitinides
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7
Q

What are the GLP-1 agonists

A
  • Exanatide

- Liraglutide

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8
Q

What are the DDP-4 inhibitors

A
  • Sitagliptin
  • Linagliptin
  • Saxagliptin
  • Alogliptin
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9
Q

What are the first gen. Sulfonylureas

A
  • Chlorpropamide
  • Tolbutamide
  • Tolazamide
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10
Q

What are the second generation Sulfonylureas?

A
  • Glipizide
  • Glyburide
  • Glimepiride
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11
Q

What are the Meglitinides

A
  • Nateglinide

- Repaglinide

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12
Q

What is the Biguanide

A

Metformin

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13
Q

What are the Thiazolidinediones?

A
  • Pioglitazone

- Rosiglitazone

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14
Q

What are the sodium-glucose co transporter 2 (SGLT2) inhibitor

A
  • Canagliflozin
  • Dapagliflozin
  • Empagliflozin
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15
Q

What are the inhibitors of alpha-glycosidases inhibitors?

A
  • Acarbose

- Miglitol

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16
Q

Which insulin pathway has effects on glucose, lipid and protein metabolism, primarily via regulation of enzyme activities

A

IR-IRS-PI3K-Akt pathway

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17
Q

Which insulin pathway controls regulation of gene transcription and cell proliferation

A

-IR-IRS-MAP kinases

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18
Q

Describe what the rapid acting insulins are used for

A
  • mutations from human sequence block assembly of dimers and hexamers-allow for faster aborption
  • Clinical use: postprandial hyperglycemia - taken before a meal
  • onset: 5-10 min
  • Duration: 1-3 hrs
  • peak: 30min - 1 hour
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19
Q

Describe short acting regular insulins

A
  • Composition: unmodified zinc insulin crystals
  • Absorption rate is slow and less predictable - form hexamers, which are too bulky to be transported via endothelium into the bloodstream
  • Clinical use: Basal insulin maintenance, overnight coverage, if for postprandial hyperglycemia - inject 45 min before the meal
  • onset: 30 min - 1 hr
  • Duration: 10 hr
  • Peak 3-5 hrs
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20
Q

Describe the intermediate acting NPH preparations

A
  • Composition: complex of protamine with zinc insulin . . protamine has to be digested by tissue proteolytic enzymes before insulin can be absorbed
  • Clinical use: basal insulin maintenance and/or overnight coverage . . use is declining and being replaced by long acting insulins
  • Onset 1-2 hours
  • Duration: 10-12 hours
  • Peak: 4-12 hours
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21
Q

Which long acting insulin: Lys 29 in B chain is myristoylated (lipid) rapidly absorbed into blood but binds strongly to albumin

A

-Detemir

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22
Q

Which long acting insulin: Amino acid substitutions in both A and B chains enhance crystal stability, change pKa of insulin - soluble at low pH (4) but precipitates at Ph 7

A

Glargine

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23
Q

Which long acting insulin peaks at 3-9 hours?

Which is peakless?

A
  • Detemir

- Glargine

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24
Q

Clinical use of long acting insulins

A

Basal insulin maintenance: 1-2 injections daily

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25
Q

What are the general clinical indications for insulin

A
  • Types 1 and 2 diabetes
  • Gestational diabetes
  • Severe Hyperkalemia
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26
Q

Describe the use of insulin in the treatment of severe hyperkalemia?

A
  • Insulin + glucose (to prevent hypoglycemic shock) + furosemide
  • Insulin (IV) rapidly activates Na/K ATPase to shift K+ from ECF into cells
  • Effect is transient (several hours)
  • K+ is eliminated from the body using loop diuretics in the meantime
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27
Q

What are the adverse effects of insulin?

A
  • Hypoglycemia
  • Lipodistrophy: localized hypertrophy/atrophy of subcutaneous fat at site of injection . .. prevented by frequently changing the site of injection or by IM injecitons
  • Resistance: Pts treated with exogenous insulin commonly develop insulin binding antibodies . . IgG antibodies can neutralize the action
  • Allergic reactions: Immediate type hypersensitivity (rare) . . due to histamine release from mast cells sensitized by anti-insulin IgE antibodies
  • Hypokalemia
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28
Q

What is the most common complications of insulin therapy

A

Hypoglycemia

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29
Q

What are the common causes of hypoglycemia from insulin use

A
  • Delay of a meal or missed meal
  • Exercise: exercised muscle consumes more glucose and Hyperemic skin leaded to enhanced rate of insulin absorption
  • Overdose of insulin
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30
Q

What are the signs of hypoglycemia?

A
  • CNS/Behavioral manifestations: confusion, bizarre behavior, seizures, coma
  • Sympathetic hyperactivity: tachycardia, palpitations, sweating, tremor
  • Parasympathetic hyperactivity: hunger, nausea
  • Patients on tight glycemic control - “hypoglycemic unawareness
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31
Q

What is the treatment of hypoglycemia?

A
  • GLucose: juice, candy (if conscious); IV glucose if unconscious
  • Diazoxide: stong hyperglycemic agent - K+ATP channel opener
  • Inhibits the release of insulin by beta cells
  • Glucagon (1 mg, sc)
32
Q

Explain the MOA of Glucagon

A
  • Gs-coupled GPCR
  • activation of adenylyl cyclase
  • Activationg of protein kinase A (PKA)
  • Activation of phosphorylase –> glycogenolysis
  • increased expression of PEPCK and Glu-6-pase–> gluconeogenesis
33
Q

Describe what the effects of glucagon are

A
  • Hepatocytes: increase glucose output, glycogen depletion . . No glycogen depletion in the skeletal muscle
  • Potent inotropic and chronotropic effect on the heart
  • GI smooth muscle relaxation
  • increase insulin release by beta cells
  • Increase release of catecholamines by chromaffin cells (contraindicated in Pheochromocytoma pts)
34
Q

Clinical uses of Glucagon

A
  • Moderate to severe hypoglycemia
  • beta blocker overdose
  • radiology
35
Q

Pharmacokinetics of Pramlintide

A
  • onset: rapid
  • Duration: 3 hr
  • peak: 20 min
36
Q

Clinical use of Pramlintide?

A
  • Type 1 diabetes
  • Type 2 diabetes pts who takes mealtime insulin therapy
  • Injected sc before meals as an adjunct to insulin
37
Q

Adverse effects of Pramlintide

A
  • GI: nausea, vomiting, diarrhea, anorexia

- Severe Hypoglycemia: especially if used together with insulin . . insulin dose should be reduced

38
Q

What is the drug interaction with Pramlintide

A

enhances effects of anticholinergic drugs in GI tract . . constipation

39
Q

Describe Exanatide

A
  • recombinant form of exendin-4, proteins from Gila monster saliva
  • only 53% homology to GLP-1 but still has agonist activity
  • Glycine substitution was made to make it less susceptible to the hydrolysis by DDP-4
  • half life: 2.4 hours
40
Q

Describe liraglutide

A
  • GLP-1 analog with 97% homology to native GLP-1
  • Lipid modified-rapidly absorbed, but binds to albumin
  • half life: 11-15 hrs
41
Q

Clinical use of long acting GLP-1 receptor agonists

A
  • The release of GLP-1 is diminished postprandially in type 2 diabetes patients –> inadequate glucagon suppression and excessive hepative glucose output
  • approved in type 3 diabetes patients who is not adequately controlled by metformin/sulfonylureas/thiazolidinediones
  • doses of other anti-diabetic meds should be reduced to avoid hypoglycemia
  • In spite of parenteral route of administration they have been gaining popularity . . improved control of hyperglycemia . . weight loss in some pts
42
Q

Most insulins are given SQ . .which can also be IV

A

Regular insulin

43
Q

What is the MOA of Amylin analog Pramlintide

A
  • inhibits glucagon secretion
  • Enhances insulin sensitivity
  • Decreases gastric emptying )slow the rate of intestinal glucose absorption)
44
Q

MOA of GLP-1

A
  • synthesized by intestinal L cells
  • Beta cell PROLIFERATION (diff. than amylin)
  • Promotes Insulin gene expression
  • promotes glucose dependent insulin secretion
  • inhibits Glucagon secretion and gastric emptying .. . like amylin
  • satiety
45
Q

What is the disadvantage of GLP-1

A

very short half life 1-2 min . . its a polypeptide

46
Q

What is the protease that cleaves GLP-1 leading to its short half life

A

DDP-4

47
Q

Describe the K+ATP channel blockers MOA

A
  • The SUR on the outside binds to the sulfonylurea receptor

- Block the K+ current through Kir6.2, inwardly rectifying potassium channel

48
Q

MAO of metformin (Biguanide)

A

Activation of AMP-dependent protein kinase

  • basically blocks mitochondrial oxidative phosphorylation leading to buildup of AMP
  • AMP dependent kinases then phosphorylate a number of targets: inhibition of lipogenesis and gluconeogenesis, increase in glucose uptake, glycolysis, and fatty acid oxidation, lower glucose levels in hyperglycemic (but not normoglycemic states), and increases insulin sensitivity
49
Q

MOA of Thiazolidinediones

A
  • Ligands of PPARgamma
  • this is a nuclear receptor expressed primarily in fat, muscle, liver tissue, and endothelium
  • increases GLUT4 in skeletal muscle and adipocytes . . so increases insulin sensitivity
50
Q

Explain what SGLT2 inhibitors do

A

decrease reabsorption of glucose so you urinate out the glucose

51
Q

MOA of alpha glycosidase inhibitors

A
  • only monosaccharides are absorbed from GI into the blood
  • Competitive inhibitor of alpha-glycosidases, a family of enzymes on the intestinal epithelium defer digestion and thus absorption of ingested starch and disaccharides
  • Lower post prandial hyperglycemia to create an insulin sparing effect
52
Q

Adverse effects of the long acting GLP-1 receptor analogs

A
  • GI: nausea, vomiting, diarrhea, anorexia
  • Lower risk of hypoglycemia vs. Pramlintide
  • It exhibits glucose dependent insulinotropism (the ability to stimulate insulin secretion during hyperglycemia but NOT during hypoglycemia)
  • Linked to cases of ACUTE PANCREATITIS and PANCREATIC CANCER
  • possible like to THYROID CANCER
53
Q

Clinical used of DDP-4 inhibitors (Gliptins)

A
  • approved as adjunctive therapy to diet and exercise in patients with type 2 diabetes
  • Used both as a monotherapy and in combo with metformin/sulfonylureas/TZDs
  • taken orally
54
Q

Adverse effects of DDP-4 inhibitors

A
  • upper respiratory infections and nasopharyngitis
  • linked to acute pancreatitis
  • Hypoglycemia (if combined with insulin secretagogues - their doses have to be adjusted)
55
Q

Compare and contrast 1st vs 2nd gen sulfonylureas

A

First: lower potency so used in high doses; developed in 50s-80s. currently used infrequently for the treatment of diabetes

  • Second: higher potency
  • developed in 80s and 90s
56
Q

Clinical use of Sulfonylureas

A

-type 2 diabetes as a monotherapy or in combination with insulin or other antidiabetic drugs

57
Q

Adverse effects of Sulfonylureas

A
  • Hypoglycemia
  • Weight gain (increased insulin release)
  • Secondary failure - patients who respond initially later cease to respond to the sulfonylurea and develop unacceptable hyperglycemia
  • Disulfiram-like effect of alcohol induced flushing
  • Dermatological and general hypersensitivity reactions: cross reactivity with other sulfonamides (sulfonamide antibiotics, Carbonic anhydrase inhibitors, Diuretics: thiazides and furosemide)
58
Q

What are the Drug interactions with sulfonylureas that enhance their hypoglycemic effect?

A
  • Displacing from binding with plasma proteins: sulfonamides, clofibrate, and salicylates
  • Enhancing the effect on K-ATP channel: ethanol
  • Inhibitin CYP enzymes: Azole antifungals, gemfibrozil, cimetidine
59
Q

What are the drug interctions with sulfonylureas that decrease their glucose lowering effect

A
  • inhibiting insulin secretion: beta-blockers, CCM
  • Antagonizing their effect of K-ATP channel: diazoxide
  • inducing hepatic CYP enzymes: phenytoin, griseofulvin, rifampin
60
Q

Clinical use of Meglitinides

A
  • Control of postprandial hyperglycemia in patients with type 2 diabetes
  • taken orally before the meal
  • Can be used either alone (to control isolated postprandial hyperglycemia) or in combination with other antidiabetic drugs
61
Q

side effects of Meglitinides

A
  • hypoglycemia
  • secondary failure
  • weight gain
62
Q

Clinical use of metformin

A

-most commonly used oral agent to treat type 2 diabetes and is generally accepted as the first line treatment for this condition

63
Q

What are the advantages of Metformin use

A
  • superior or equivalent glucose lowering efficacy compared to other oral meds
  • Does not cause hypoglycemia
  • does not cause weight gain
  • taken orally
  • can be used either alone or in combination with other oral agents
  • In clinical trials decreased the risk of both macro- and microvascular complications in diabetic patients
64
Q

Pharmacokinetics of metformin

A
  • half life: 1.5-3 hours
  • not bound to plasma proteins
  • Not metabolized
  • Excreted unchanged by kidneys
65
Q

Adverse effects and contraindications of metformin

A
  • Most common: GI complications - anorexia, vomiting, nausea, diarrhea, abdominal discomfort
  • Decreased absorption of vit B12
  • Lactic acidosis, especially under conditions of hypoxia, renal and hepatic insufficiency
  • Contraindicated in conditions predisposing to tissue hypoxia (HF, COPD), renal failure, chronic alcoholism, and cirrhosis
66
Q

What CYPs metaboliz pioglitazone?

A

CYP2C8 and 3A4

67
Q

What CYPs metabolize Rosiglitazone?

A

CYP2C8 and 2C9

68
Q

important pharmacokinetic features of Thiazolidinediones?

A
  • taken orally once daily
  • changes gene expression so full effects develop 1 to 3 months later
  • metabolized in liver
  • safe to administer to pts with renal failure
69
Q

Clinical use of Thiazolidinediones?

A
  • Type 2 diabetes alone or in combination with other antidiabetic drugs
  • Shown to delay progression from prediabetes to type 2 diabetes
  • Euglycemic drugs (no hypoglycemia with used alone)
70
Q

Adverse effects of Thiazolidinediones

A
  • Weight gain (incidence doubles if with insulin)
  • Edema (also doubles if with insulin)
  • Exacerbation of heart failure: contraindicated in NTHA class III or IV HF
  • Link to increased risk of BLADDER CANCER (piogliazone)
  • Osteoporosis: bone fractures (especially in post menopausal women
71
Q

What are the other effects of SGLT2 inhibitors

A
  • cause osmotic diuresis
  • induces weight loss
  • reduce blood pressure
  • reduce plasma levels of uric acid
  • Do NOT cause hypoglycemia when used alone
72
Q

Clinical used of SGLT2 inhibitors?

A
  • Adjunct to diet and exercise in adults with type 2 diabetes
  • take orally before the first meal once a da
  • in patients with hypovolemia, this condition should be corrected before the start of therapy
73
Q

Adverse effects of SGLT2 inhibitors

A
  • Hypotension
  • hypovolemia: orthostatic hypotension and dizziness, syncope
  • Genital (mycotic) and urinary tract infections: can lead to life threatening blood infections (urosepsis) and kidney infections (pyelonephritis)
  • Hypoglycemia if combined with insulin or insulin secretegogues
  • increased LDL-C
  • renal function impairment: induce fall in glomerular filtration rate and increase plasma creatinine
  • Hyperkalemia (especially in patients with impaired renal funcitons and those taking ACEIs, ARB, and K+ sparing diuretics
  • development of ketoacidosis
74
Q

Clinical use of alpha-Glycosidase inhibitors

A
  • Type 2 diabetes as monotherapy or in combo with other oral antidiabetic agents or insulin
  • Taken orally at mealtime
  • Do NOT cause hypoglycemia when used alone
  • Do NOT cause weight gain
75
Q

Adverse effects of alpha Glycosidase inhibitors

A
  • Most common: malabsorption, flatulence, and abdominal bloating
  • hypoglycemia has been described when combined with insulin or insulin secretegogues
76
Q

Drug interactions with Alpha Glycosidase inhibitors

A

-Decrease absorption of digoxin and propranolol and ranitidine

Endocrine 2 (10 decks)

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