Antidiabetics Flashcards

1
Q

Types of insulin

A

Human, Porcine, Bovine

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2
Q

Examples of Insulin

A

Neutral Protamine Hagedorn (NPH)
Regular
Lente
Ultralent

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3
Q

Common mixture of insulin

A

70% NPH + 30% Regular

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4
Q

Ultra-short acting insulin analogues

A

Aspart and Glulisine- 3-5

Lispro-2-5

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5
Q

Short Acting

A

Regular (soluble crystalline)-5-8

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6
Q

Intermediate

A

NPH (isophane)-18-24

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7
Q

Long acting

A

Detemir-20-22

Glargine-18-24

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8
Q

Ultra long acting

A

Degludec

>40

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9
Q

Administration of most insulin analouges

A

SUBCUTANEOUS

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10
Q

Analogs that increase in duration when dose is increased

A

NPH, Regular

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11
Q

Amino acid PROLINE at position 28 is replaced by Aspartic Acid

A

Aspart

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12
Q

Proline at B 28 interchanged with Lysine at B 29

A

Lispro

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13
Q

Glutamine for Proline

A

Glulisine

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14
Q

Quickly dissociates into monomers therefore faster absorption. Also the shortest acting of them all

A

Lispro

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15
Q

Difference long acting in terms of dissociation

A

It is bound together in the solution that’s why it is slowly dissociating

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16
Q

Instantl converted to monomers if given IV, short acting

A

Regular

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17
Q

Added to Regular insulin to improve stability and shelf life

A

Zinc

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18
Q

Delayed action so that insulin and protamine in an uncomplexed form

A

NPH

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19
Q

Long acting insulin are also called

A

Peakless- broad plasma concentration plateau

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20
Q

Responsible for controlling fasting blood sugar

A

Long acting

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21
Q

Responsible for controlling postprandial blood sugar

A

Short acting

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22
Q

Given a px whose on Glargine (taken before bedtime) and Lispro (taken before breakfast, lunch and dinner) who is complaining of palpitation, tremors and hunger pangs before lunch time. What is your management?

A

Reduce Lispro before breakfast

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23
Q

Common multi dose insulin regimen

A
  1. Short acting before meals and long acting at nighttime
  2. Short acting or regular and NPH before breakfast and supper
  3. Insulin in bolus
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24
Q

Insulin ADR

A
Hypoglycemia
Lipodystrophy
Allergy
Insulin Resistance
Weight gain
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25
Q

Normal RBS

A

140mg/dL

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26
Q

Insulin secretagogues

A

Sulfonylureas

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27
Q

Glibenclamide

A

2nd Generation Sulfonylurea

  • 1st Gen- amides
  • 2nd gen- ides
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28
Q

Secretagogues MOA

A

Closing of ATP-dependent K channel, thereby depolarizing the membrane to increase insulin release

29
Q

Secretagogue with longest duration of action

A

Chlorpropamide (60 hrs)

30
Q

2nd generation secretagogues DOA

A

10-24

31
Q

Chlorpropamide ADR

A

Hypoglycemia
Hyponatremia (SIADH)
Disulfiram-like rxns

32
Q

Meglitinides (Repa-, Nate-)

A

Less Hypoglycemic effects

WEIGHT GAIN

33
Q

Biguanide

A

Metformin

34
Q

Metformin does not cause hypoglycemia

A

Euglycemic

35
Q

Metformin effects

A

Dec gluconeogenesis

Inc glucose uptake

36
Q

Metformin MOA

A

Activates AMP PK for insulin signaling

37
Q

First line drug for DM type 2

A

Metformin

38
Q

Other indications of metformin

A

PCOS

39
Q

Metformin ADR

A

GI disturbances
B12 Deficiency
Lactic acidosis
CI: RENAL INSUFFICIENCY

40
Q

Oral agent that causes EDEMA and WEIGHT GAIN

a. Pioglitazone
b. Repaglinide
c. Insulin

A

Pioglitazone

  • Repaglinide- weight gain only
  • Insulin- causes both but not oral
41
Q

Pioglitazone MOA

A

Increase peripheral glucose uptake

PPAR gamma agonists

42
Q

LDL effects of TZDs

A

Pioglitazone- Dec

Rosiglitazone- Inc

43
Q

TZDs ADR

A

Hepatotoxicity (Troglitazone)
WEight gain and Edema
MI risk (Rosi)

44
Q

Acarbose MOA

A

Delay CHO absorption by inhibiting glucosidase actions

45
Q

Acarbose is an

A

Alpha-glucosidase Inhibitor does not cause Weight Gain

46
Q

Acarbose ADR

A

Flatulence

47
Q

Incretins

A

Intestinal Secretion of Insulin

48
Q

Secretes incretin

A

L cells

49
Q

Incretin effect

A

Glucose-dependent- more potent release of insulin on ingested food than IV glucose

50
Q

Disease where incretin effect is greatly reduced or absent

A

DM 2

51
Q

First FDA approved Incretin mimetic

A

Exenatide

52
Q

Exenatide MOA

A

GLP-1 agonist

53
Q

Disadvantages of Exenatide

A

Injected
GI disturbances
Pancreatitis

54
Q

advantages of Exenatide

A
lack of hypoglycemia
Weight Loss (Laklak na ng Exenatide)
55
Q

Why is GLP-1 limited thus requires continuous admnistration?

A

Rapid degradation by the ubiquitous enzyme dipeptidyl eptidase-IV (DPP IV)

56
Q

DPP-IV inhibitors

A

-gliptins

57
Q

gliptins

A

Oral

Euglycemic

58
Q

Daily GFR of 180L/day, how much glucose is reabsorbed?

A

162g

59
Q

N: plasma blood glucose concentration

A

5.6 mmol/L

60
Q

SGLT 1

A

10%

Straight (S3)

61
Q

SGLT 2

A

90%

Convoluted (S1)

62
Q

SGLT 2 inhibitors

A

inhibits renal reabsorption of glucose. Favors glucose excretion

63
Q

Advantages of SGLT 2 inhitors

A

May lower blood pressure

64
Q

Amylin analog

A

Pramlintide

65
Q

Pramlintide MOA

A

mimics amylin (secreted with insulin by B cells) and suppresses glucagon secretion, dec HGO and dec insulin demand

66
Q

Glucagon other uses

A

Treatment of Beta blocker poisoning due to its chronotropic and inotropic effects

67
Q

Hypoglycemia with reaction of two drugs

A

Glibenclamide and Repaglinide

68
Q

Optimum treatment to a patient with elevated BS and will not result to weight gain

A

METFORMIN AND DAPAGLIPLOZIN