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Spring 2018 Pharm Exam 2 > Lecture 2: Drugs for DM > Flashcards

Lecture 2: Drugs for DM Flashcards

1
Q

What is the primary Tx for Type 1 DM

A

insulin replacement

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2
Q

What is the MC form of insulin used today

How is insulin normally given
- how given in emergency?

A

Recombinant products

Normally insulin injected SC
- in emergency: IV or IM

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3
Q

How are insulin preps classified?

A

by duration of action

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4
Q

What 3 types are ULTRA short acting insulin

A
  1. Lispro
  2. Aspart
  3. Glulisine
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5
Q

What 3 types are rapid short acting insulin

A
  1. standard insulin
  2. humulin-R
  3. Purified insulin
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6
Q

What 2 types are intermed acting insulin

A
  1. novolin-N

2. humulin-N

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7
Q

What 2 types are long acting insulin?

A
  1. Detemir

2. Glargine

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8
Q

How does glucose uptake/peak differ from short and long acting?

A

Short acting

  • quick glucose uptake
  • immed peak

Long acting
- NO PEAK

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9
Q

When should short acting insulin be used?

long acting?

A

short acting –> at mealtime

long acting –> overnight

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10
Q

definition of Dawn Effect in DM

- d/t?

A

increase in AM blood glucose d/t overnight insulin dosing and cortisol

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11
Q

2 ways to monitor response to insulin replacement

A
  1. Blood glucose

2. Glycated Hb

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12
Q

What is the major AE a/w insulin Tx?

What can be given to reverse this?

A

HYPOglycemia ( <70) - can be fatal

Give glucose or glucagon to reverse hypoglycemia

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13
Q

What are 2 common causes of HYPOglycemia w/insulin Tx

What is hypoglycemia a/w later in life?

A
  1. Too much insulin given
  2. insulin given at incorrect time

A/w dementia later in life

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14
Q

Where in the body does physiologic insulin go 1st?

Insulin replacement go 1st?

A

physiologic –> Liver

insulin replacement –> circulation

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15
Q

Other AEs a/w insulin Tx

Note: no risk in pregnancy

A
  1. Hypersensitivity rxns (less w/recombinant)

2. lipoatrophy or lipohypertrophy

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16
Q

2 pathophys probs in Type 2 DM

A
  1. insulin resistance
  2. impaired insulin secretion

incr: hepatic gluc production & glucagon
decr: gluc utilization & secretion

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17
Q

What is the 1st line tx for Type 2 DM

is insulin typically used initially for Tx of type 2 DM

A

lifestyle modifications
- exercise and wt control

No insulin not usu used initially

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18
Q

W/severe hypoglycemia how do you know whether its d/t OD of self admin insulin or insulin secreting tumor?

A

C-peptide

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19
Q

7 Classes of drugs that Tx Type 2 DM

A
  1. Biguanides
  2. Classic Secretagogues
  3. Thiazolidinediones
  4. Renal SGLT-2 inhibitors
  5. GLP-1 agonists
  6. DPP-4 inhibitors
  7. Alpha-glucosidase Inhibitors
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20
Q

What type of drugs are Biguanides?

prototype drug for Biguanides?

A

insulin sensitizers –> enhances insulin’s effects

Metformin

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21
Q

MOA for Metoformin?

end results?

A

Activates AMPK

incr: gluc uptake and FA oxidation
decr: gluconeogenesis and lipogenesis

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22
Q

how can you incr the activity of AMPK

A

exercise

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23
Q

What is metformin often used in combo w/ and why?

A

often in combo w/PO anti-diabetic meds –> additional glucose control

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24
Q

GI effects of metformin = N/V/D and metallic taste

- dose effect and how long they last?

A

Dose-dependent and transient

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25
Q

Who is metformin CI in?

A

pts w/ renal dysfx or severe liver dz

26
Q

What can occur if metformin given to renal impaired pt

why must d/c metformin before radiographic procedures w/contrast

A

renal impaired–> Lactic acidosis

d/c before proced –> may cause rapid decline in renal fxn

27
Q

What is metformin 1st line for?

A

Type 2 DM

28
Q

3 benefits of metoformin?

A
  1. Does NOT induce hypoglycemia
  2. NO wt gain
  3. inhibits microvascular complications
29
Q

Two type of Classic secretagogues

general MOA for them?
hence what do both require?

A
  1. Sulfonylureas
  2. Non-sulfonylurea secretagogues

Mimic glucose –> bind/inhibit ATP sensitive K channel –> block K efflux –> depol –> incr insulin rel
- requires fxnl beta cells

30
Q

Prototype drug for Sulfonylureas

A

Glipizide

31
Q

What does Glipizide not affect?

A

insulin resis/sensitivity

32
Q

2 major AEs a/w Glipizide

A
  1. HYPOglycemia

2. Wt gain

33
Q

What pts is Glipizide CI in? cautioned use in?

A

CI - pts w/liver or renal dz

caution - elderly, cardiac pts

34
Q

2 major results of drug interactions w/Glipizide

A
  1. enhanced HYPOglycemic effect (w/decr metab, excretion, protein binding)
  2. compromised glucose lowering effect (w/incr metab, excretion, inhibition of insulin secretion)
35
Q

prototype drug for Non-sulfonylurea secretagogues/Meglitinides?

A

Repaglitinide

36
Q

how are Non-sulfonylurea secretagogues similar to sulfonylureas and how different (5)?

A

same MOA

Non-sulfonylurea secretagogues

  • share 2 binding sites w/SU but diff kinetics
  • shorter acting (give right before meal)
  • lower risk of HYPOglycemia
  • less wt gain
  • caution w/liver dz (CI in SU)
37
Q

what are two ways drug interactions/enhancement of HYPOglycemia occurs w/Non-sulfonylurea secretagogues

A
  1. drugs that displacement from protein binding sites

2. drugs interfere w/metab

38
Q

What types of drugs are Thiazolidinediones?

A

insulin sensitizers (like Biguanides)

39
Q

prototype drug for Thiazolidinediones?

A

Pioglitazone

40
Q

general MOA for Pioglitazone

what alters expression of insulin responsive genes that results in the MOA?

A

incr insulin sensitivity in target tissues

PPAR-gamma ligands
Peroxisome Proliferator-Activated Rec

41
Q

major benefit of Pioglitazone?

A

NOT HYPOglycemic

42
Q

Effect of Pioglitazone on hepatic glucose output, gluc utilization and FFA

A

decr hepatic glucose output and FFA

incr gluc utilization

43
Q

2 major AEs a/w Pioglitazone

Other AEs:

  1. decr bone density w/chronic use
  2. incr risk of HF, bladder CA?
  3. liver failure (caution in liver dz)
A
  1. Fluid retention

2. Wt gain

44
Q

prototype drug for GLP-1 rec agonists

A

Exenatide (injectable)

45
Q

MOA for Exenatide? result?

Others:
decr post prandial gluc rel and hepatic fat acculm

A

incr glucose dep insulin secretion–> less chance of HYPOglycemia

46
Q

How does Exenatide help facilitate wt LOSS?

A

slows gastric empty/incr satiety

47
Q

What AE a/w Exenatide decr w/continued use and leads to acute renal failure

Other AE: acute pancreatitis

A

GI SEs: N/V/D

vomiting a/w acute renal failure

48
Q

when is there a higher risk of HYPOglycemia w/ Exenatide?

A

when given w/insulin secretagogues

49
Q

What pts is Exenatide CI in?

A

gastroparesis

50
Q

Prototype drug for DPP-4 inhibitors

dipeptidyl peptidase

A

Sitagliptin

note: wt neutral

51
Q

2 MOA for Sitagliptin

A
  1. prolongs action of endogenous GLP-1

2. incr glucose mediated insulin secretion

52
Q

4 major AEs a/w Sitagliptin?

Others:

  1. acute pancreatitis
  2. Hypersensitivity rxns
  3. unknown long term safety
A
  1. incr risk hypoglycemia w/insulin secretagogues
  2. cleavage not specific to incretins
  3. hepatic failure (can be fatal)
  4. may cause severe joint pain
53
Q

prototype drug for alpha-glucosidase inhibitors

A

acarbose (NOT absorbed)

54
Q

2 MOA of acarbose?

A
  1. inhibits alpha-glucosidase –> slows carb digestion–> decr GI gluc absorption
  2. decr postprandial glycemia –> must take w/meal
55
Q

3 AEs a/w acarbose that is alleviated w/dose titration and continued use?

Others:

  1. incr LFTs/hepatic failure
  2. incr risk hypoglycemia w/SU or insulin
A

abd pain, diarrhea, flatulence

56
Q

CI for acarbose

A

Chronic intestinal dz

57
Q

What is prototype drug for Renal SGLT-2 inhibitors (glucose transport inhibitors)

A

Canagliflozin

not FDA approved

58
Q

MOA for Canagliflozin

A

inhibits SLGT-2 (Na dep glucose co-transporter in kidney) –> suppresses renal gluc abs –> lowers blood glucose

59
Q

what is Canagliflozin metab by? result?

A

metab by UDP-GT inducers –> decr blood levels of drug

60
Q

4 major AEs a/w Canagliflozin?

Others =HYPER: P, Mg, K

A
  1. genital myocotic inf
  2. reccurent STIs
  3. unknown long term safety –> incr risk of bone fx?
  4. Ketoacidosis
61
Q

POSSIBLE benifits of Canagliflozin

A
  1. facilitate wt loss

2. improve health in CV pts (excrete more Na–> decr BV)

Spring 2018 Pharm Exam 2 (6 decks)

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