Drugs used in die-beetus

Question 1

What are the rapid acting insulins

Answer 1

Aspart
Lispro
Glulisine

Question 2

What is the clinical use of rapid acting insulin

Answer 2

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

Question 3

What is the short acting insulin

Answer 3

Regular insulin

Question 4

What are the clinical uses of regular insulin

Answer 4

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

Question 5

What is the intermediate acting insulin

Answer 5

NPH insulin

Question 6

Composition of NPH insulin

Answer 6

Complex of protamine with zinc insulin

Question 7

Clinical use of NPH insulin

Answer 7

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

Question 8

What are the long acting insulins

Answer 8

Detemir

Glargine

Question 9

Clinical use of long acting insulins

Answer 9

Basal insulin maintenance (1‐2 sc injections daily)

Question 10

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

Answer 10

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

Question 11

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

Answer 11

– 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

Question 12

Insulin delivery systems

Answer 12

Standard- subq injection
Portable pen injectors
Insulin pumps

Question 13

What is the most common complication of insulin therapy

Answer 13

hypoglycemia

Question 14

Common causes of hypoglycemia

Answer 14

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

Question 15

signs of hypoglycemia

Answer 15

– 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”

Question 16

Treatment of hypoglycemia

Answer 16

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

Question 17

MOA of amylin

Answer 17

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

Question 18

What is the amylin analog drug

Answer 18

Pramlintide

Question 19

Clinical use of Pramlintide

Answer 19

– 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

Question 20

Adverse effects of pramlintide

Answer 20

– GI: nausea, vomiting, diarrhea, anorexia

– Severe hypoglycemia – if used together with insulin

Question 21

Drug interactions of pramlintide

Answer 21

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

Question 22

What are incretins

Answer 22

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

Question 23

What is GLP-1 synthesized by?

Answer 23

intestinal L cells

Question 24

What does GLP-1 promote

Answer 24

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

Question 25

What does GLP-1 inhibit

Answer 25

glucagon secretion gastric emptying not an effective drug bc short half life

Question 26

What are the long acting GLP1 receptor agonists What are their half lives?

Answer 26

Exenatide (2.4 hr) | Liraglutide (11-15 hr)

Question 27

Adverse effects of the GLP-1 receptor agonists

Answer 27

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

Question 28

GLP-1 agonists are approved for which patients

Answer 28

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

Question 29

suffix for DPP-4 inhibitors

Answer 29

-gliptin

Question 30

MOA of DPP-4 inhibitors

Answer 30

* Increase levels of GLP-1 to enhance its interactions with the cognate receptor * Effects are similar to those of GLP-1 agonists

Question 31

What is DPP-4

Answer 31

A serine protease that degrades GLP-1 and other incretins

Question 32

Clinical use of the gliptins (DPP-1 inhibitors)

Answer 32

– 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

Question 33

Adverse effect of gliptins

Answer 33

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

Question 34

Classes of K+ atp channel blockers

Answer 34

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

Question 35

first gen sulfonylureas

Answer 35

-mide – Chlorpropamide – Tolbutamide – Tolazamide

Question 36

second gen sulfonylureas

Answer 36

– Glipizide – Glyburide – Glimepiride

Question 37

Meglitinides

Answer 37

-glinide – Nateglinide – Repaglinide

Question 38

MOA of K+ atp channel blockers

Answer 38

* Binding to SUR1 – sulfonylurea receptor | * Blocking K+ current through Kir6.2 inwardly rectifying potassium channel

Question 39

Clinical use of sulfonylureas

Answer 39

Type 2 diabetes as a monotherapy or in | combination with insulin or other anti-diabetic drugs

Question 40

Adverse effects of sulfonylureas

Answer 40

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

Question 41

Sulfonylurea drug interactions that enhance their hypoglycemic effect

Answer 41

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

Question 42

Sulfonylurea drug interactions that decrease their hypoglycemic effect

Answer 42

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

Question 43

Clinical use of meglitinides

Answer 43

– 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

Question 44

Adverse effects of meglitinides

Answer 44

– Hypoglycemia – Weight gain – Secondary failure

Question 45

MOA of metformin

Answer 45

– Activation of AMP-activated protein kinase

Question 46

What is the first line treatment for T2DM

Answer 46

Metformin

Question 47

Advantages of metformin

Answer 47

• 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

Question 48

Adverse effects of metformin

Answer 48

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

Question 49

Contraindications of metformin

Answer 49

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

Question 50

What are the thiazolidinediones

Answer 50

-glitazone Pioglitazone Rosiglitazone

Question 51

MOA of glitazones

Answer 51

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

Question 52

Adverse effects of glitazones

Answer 52

Weight gain Edema Exacerbation of heart failure Osteoporosis

Question 53

What is the suffix for SGLT2 inhibitors

Answer 53

-flozin

Question 54

MOA of SGLT2 inhibitors

Answer 54

– 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

Question 55

Adverse effects of SGLT2 inhibitors

Answer 55

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

Question 56

What are the α-glycosidase inhibitors

Answer 56

Acarbose | Miglitol

Question 57

MOA of α-glycosidase inhibitors

Answer 57

– 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

Question 58

Adverse effects of α-GLYCOSIDASE INHIBITORS

Answer 58

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