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endorepro remediation > Drugs used in die-beetus > Flashcards

Drugs used in die-beetus Flashcards

1
Q

What are the rapid acting insulins

A

Aspart
Lispro
Glulisine

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2
Q

What is the clinical use of rapid acting insulin

A

– Postprandial hyperglycemia – taken before the meal (as sc injections only

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3
Q

What is the short acting insulin

A

Regular insulin

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4
Q

What are the clinical uses of regular insulin

A

– Basal insulin maintenance
– Overnight coverage
– If for postprandial hyperglycemia – inject 45 min before the meal
– Can be injected intravenously in urgent situations

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5
Q

What is the intermediate acting insulin

A

NPH insulin

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6
Q

Composition of NPH insulin

A

Complex of protamine with zinc insulin

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7
Q

Clinical use of NPH insulin

A

-Basal insulin maintenance and/or overnight
coverage
– Use is declining – is being replaced by long-acting insulins

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8
Q

What are the long acting insulins

A

Detemir

Glargine

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9
Q

Clinical use of long acting insulins

A

Basal insulin maintenance (1‐2 sc injections daily)

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10
Q

What is the importance of tight glycemic control with insulin in diabetes

A
  • Improves survival
  • Reduces diabetic complications
  • Has been shown to be effective in multiple clinical trials, especially in patients with type 1 diabetes
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11
Q

What is the use of insulin in the treatment of severe hyperkalemia

A

– Insulin + glucose (to prevent hypoglycemic shock) + furosemide
– Insulin (i.v.) rapidly activates Na+/K+-ATPase to shift K+ from extracellular fluid into cells
– Effect is transient (several hours)
– K+ is eliminated from the body using loop diuretics in the meantime

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12
Q

Insulin delivery systems

A

Standard- subq injection
Portable pen injectors
Insulin pumps

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13
Q

What is the most common complication of insulin therapy

A

hypoglycemia

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14
Q

Common causes of hypoglycemia

A

– Delay of a meal or a missed meal
– Exercise
– Overdose of insulin

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15
Q

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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16
Q

Treatment of hypoglycemia

A

– Glucose or sucrose (juice, candy, etc. if conscious; I.V. glucose if unconscious)
– Glucagon (1 mg, sc)

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17
Q

MOA of amylin

A

Enhances the action of insulin via the following:

  • Inhibition of glucagon secretion
  • Decreased gastric emptying (slows the rate of intestinal glucose absorption)
  • Causes a feeling of satiety
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18
Q

What is the amylin analog drug

A

Pramlintide

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19
Q

Clinical use of Pramlintide

A

– Type 1 diabetes
– Type 2 diabetes patients who takes mealtime insulin therapy
– Injected sc before meals as an adjunct to insulin therapy to control postprandial hyperglycemia

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20
Q

Adverse effects of pramlintide

A

– GI: nausea, vomiting, diarrhea, anorexia

– Severe hypoglycemia – if used together with insulin

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21
Q

Drug interactions of pramlintide

A

Enhances effects of anticholinergic drugs on GI tract (i.e. constipation)

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22
Q

What are incretins

A

group of gastrointestinal hormones that cause a decrease in blood glucose levels

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23
Q

What is GLP-1 synthesized by?

A

intestinal L cells

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24
Q

What does GLP-1 promote

A
  • β‐cell proliferation
  • Insulin gene expression
  • Glucose‐dependent insulin secretion
25
Q

What does GLP-1 inhibit

A

glucagon secretion
gastric emptying

not an effective drug bc short half life

26
Q

What are the long acting GLP1 receptor agonists

What are their half lives?

A

Exenatide (2.4 hr)

Liraglutide (11-15 hr)

27
Q

Adverse effects of the GLP-1 receptor agonists

A

– GI: nausea, vomiting, diarrhea, anorexia
– Hypoglycemia (lower risk of hypoglycemia as
compared to insulin and sulfonylureas)

28
Q

GLP-1 agonists are approved for which patients

A

Approved in type 2 diabetes patients who is not adequately controlled by metformin/sulfonylureas/thiazolidinediones

29
Q

suffix for DPP-4 inhibitors

A

-gliptin

30
Q

MOA of DPP-4 inhibitors

A
  • Increase levels of GLP-1 to enhance its interactions with the cognate receptor
  • Effects are similar to those of GLP-1 agonists
31
Q

What is DPP-4

A

A serine protease that degrades GLP-1 and other incretins

32
Q

Clinical use of the gliptins (DPP-1 inhibitors)

A

– Approved as adjunct therapy to diet and exercise
in patients with type 2 diabetes
– Used both as a monotherapy and in combination with metformin/sulfonylureas/TZDs
– Taken orally

33
Q

Adverse effect of gliptins

A

Hypoglycemia (if combined with insulin secretagogues – their doses have to be adjusted)

34
Q

Classes of K+ atp channel blockers

A
  1. 1st generation sulfonylureas
  2. 2nd generation sulfonylureas
  3. non-sulfonylureas (meglitinides)
35
Q

first gen sulfonylureas

A

-mide

– Chlorpropamide
– Tolbutamide
– Tolazamide

36
Q

second gen sulfonylureas

A

– Glipizide
– Glyburide
– Glimepiride

37
Q

Meglitinides

A

-glinide

– Nateglinide
– Repaglinide

38
Q

MOA of K+ atp channel blockers

A
  • Binding to SUR1 – sulfonylurea receptor

* Blocking K+ current through Kir6.2 inwardly rectifying potassium channel

39
Q

Clinical use of sulfonylureas

A

Type 2 diabetes as a monotherapy or in

combination with insulin or other anti-diabetic drugs

40
Q

Adverse effects of sulfonylureas

A

– Hypoglycemia
– Weight gain (due to increased insulin release)
– Secondary failure – patients who respond initially later cease to respond to sulfonylureas and
develop unacceptable hyperglycemia

41
Q

Sulfonylurea drug interactions that enhance their hypoglycemic effect

A

– Displacing from binding with plasma proteins: sulfonamides, clofibrate, salicylates and other NSAIDs
– Ethanol
– Inhibiting CYP enzymes: azole antifungals,
gemfibrozil, cimetidine, etc.

42
Q

Sulfonylurea drug interactions that decrease their hypoglycemic effect

A

Inhibiting insulin secretion: beta-blockers, CCBs
– Inducing hepatic CYP enzymes: phenytoin,
griseofulvin, rifampin, etc.

43
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

44
Q

Adverse effects of meglitinides

A

– Hypoglycemia
– Weight gain
– Secondary failure

45
Q

MOA of metformin

A

– Activation of AMP-activated protein kinase

46
Q

What is the first line treatment for T2DM

A

Metformin

47
Q

Advantages of metformin

A

• Superior or equivalent glucose-lowering efficacy compared to other oral medications
• 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

48
Q

Adverse effects of metformin

A

– Most common: GI complications – anorexia, vomiting, nausea, diarrhea, abdominal discomfort
– Lactic acidosis, especially under conditions of
hypoxia, renal and hepatic insufficiency

49
Q

Contraindications of metformin

A

– Contraindicated in conditions predisposing to
tissue hypoxia (HF, COPD), renal failure, chronic
alcoholism and cirrhosis, etc.)

50
Q

What are the thiazolidinediones

A

-glitazone

Pioglitazone
Rosiglitazone

51
Q

MOA of glitazones

A

– Ligands of peroxisome proliferator-activated receptor-gamma (PPARγ)
– PPARγ is a nuclear receptor expressed primarily in fat, muscle, liver tissue, and endothelium

52
Q

Adverse effects of glitazones

A

Weight gain
Edema
Exacerbation of heart failure
Osteoporosis

53
Q

What is the suffix for SGLT2 inhibitors

A

-flozin

54
Q

MOA of SGLT2 inhibitors

A

– Kidneys filter 160 to 180 g of glucose per day
– Glucose is reabsorbed in the proximal tubule primarily by SGLT2
– Gliflozins inhibit this transporter to increase glucose excretion and to reduce hyperglycemia

55
Q

Adverse effects of SGLT2 inhibitors

A

hypotension
hypovolemia (fainting dizziness, syncopy)
Genital infections and UTIs
hypoglycemia

56
Q

What are the α-glycosidase inhibitors

A

Acarbose

Miglitol

57
Q

MOA of α-glycosidase inhibitors

A

– Competitive inhibition of α-glycosidases, a family of enzymes on the intestinal epithelium defer digestion and thus absorption of ingested starch and disaccharides
– Lower postprandial hyperglycemia to create an insulin-sparing effect

58
Q

Adverse effects of α-GLYCOSIDASE INHIBITORS

A

– Most common: malabsorption, flatulence, diarrhea, and abdominal bloating
– Hypoglycemia has been described when
combined with insulin or insulin secretagogues

endorepro remediation (21 decks)

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