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Endocrinology > Pharm 39 Objectives > Flashcards

Pharm 39 Objectives Flashcards

1
Q

What is the type of insulin deficiency in type-1 DM?

A
  • Lack proper B-cell function and insulin deficient

- Insulin is life-saving drug for pts with type 1

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2
Q

What is the type of insulin deficiency in type-2 DM?

A
  • Insulin resistant - suboptimal response to insulin

- Insulin can be administered to overcome resistance and promote increased cellular glucose uptake

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3
Q

What is Amylin and where is it produced and released by?

A
  • “satiety” (fullness) hormone

- Produced in and released by pancreatic B-cell and co-secreted w/insulin

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4
Q

What are the physiologic actions of Amylin (pharm name Pramlintide)?

A
  • Reduced appetite
  • Decreased gastric motility/slows gastric emptying
  • Lowers post-prandial glucose peak
  • Decrease glucagon release
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5
Q

What is Glucagon secreted by?

A

Secreted by pancreatic a-cells

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6
Q

What are the physiologic actions of Glucagon?

A
  • SubQ injection to increase glucose during hypoglycemic emergencies
  • Relaxation of smooth muscle in GI tract
  • Positive inotropic and chronotropic effect of the heart.
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7
Q

What is Glucagon-like peptide (GLP) secreted by?

A

Secreted by the intestinal L-cells, not the pancreas.

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8
Q

What are the physiologic actions of GLP 1?

A
  • Inhibits glucagon secretion
  • Potent stimulator of insulin syntheses and release
  • Slows gastric emptying and has anorectic effect
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9
Q

What are the physiologic actions of GLP 2?

A

Primary GI effects

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10
Q

Somatostatin causes widespread inhabitation of what?

A

Inhibition of endocrine and exocrine fxn of pancreas, gall bladder, and gut

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11
Q

Somatostatin inhibits secretion of what hormones?

A
  • Growth hormone
  • Glucagon
  • TSH
  • Insulin
  • LH
  • Vasoactive intestinal peptide (VIP)
  • PTH
  • Calcitonin
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12
Q

What are the similarities of the various insulin preparations?

A
  • All “human insulin”
  • Equipotent (ie: equal serum concentration reduce serum glucose similarly)
  • All given by injection (most are subQ injection, except insulin-R is given IV)
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13
Q

What are the differences of the various insulin preparations?

A

Pharmacokinetic properties differ based on onset rapidity and duration of action.

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14
Q

What is rapid acting insulin good for?

A

Good for post-prandial glucose spikes (ie: meal time coverage)

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15
Q

What is the onset, peak, and duration of rapid acting insulin?

A
  • Onset: 5-15 min
  • Peak: 1-2 hrs
  • Duration: 3-4 hrs
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16
Q

What is the onset, peak, and duration of short acting SubQ insulin?

A
  • Onset: 15-60 min
  • Peak: 2-4 hrs
  • Duration: 4-8 hrs
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17
Q

What is the onset, peak, and duration of short acting IV insulin?

A
  • Onset: <15 min
  • Peak: 15-30 min
  • Duration: 5-15min
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18
Q

What is the onset, peak, and duration of intermediate acting insulin?

A
  • Onset: 2-4 hrs
  • Peak: 4-12 hrs
  • Duration: 10-20 hrs
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19
Q

What is the onset, peak, and duration of long acting insulin?

A
  • Onset: 1-3 hrs
  • Peak: no peak?
  • Duration: 18-24+ hrs
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20
Q

What are the generic rapid acting insulin names?

A
  • Lispro
  • Aspart
  • Glulisine
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21
Q

What is the generic short acting insulin names?

A
  • Regular insulin (SubQ)

- Regular insulin (IV)

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22
Q

What is the generic intermediate acting insulin name?

A
  • Neutral Protamine Hagedorn (NPH)
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23
Q

What is the generic long acting insulin names?

A
  • Detemir
  • Glargine
  • Degludec
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24
Q

In general terms what modifications are made to make a rapid-acting insulin faster acting than regular insulin?

A
  • Longer acting is d/t slow release from the injection site

- Rapid-acting inhibits hexamer formation allowing it to produce a rapid-acting effect from the injection site.

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25
Q

What 2 diabetes medication classes are most likely to incite hypoglycemia?

A
  • Insulin

- Sulfonylureas (2nd gen agents higher potency compared to 1st)

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26
Q

How do you manage a hypoglycemic episode in a conscious pt?

A
  • Oral glucose dose of 15 gram
  • Monitor BD and repeat dose after 15 min if necessary
  • Glucagon may be given to a conscious patient, but oral glucose is preferred.
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27
Q

How do you manage a hypoglycemic episode in an unconscious pt?

A
  • Subcutaneously-injected glucagon
  • Once the patient is conscious, the patient should receive some glucose supplementation to replenish hepatic glycogen stores.
  • Intravenous glucose (a.k.a., “dextrose”) is an acceptable alternative to glucagon when practical.
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28
Q

What step of insulin release is the mechanism of action of the sulfonylurea (and other secretagogue) drugs?

A

Closing the ATP sensitive potassium channel

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29
Q

What is the MOA of Metformin (Biguanides)?

A
  • “insulin sensitizer”
  • Decreases hepatic glucose production
  • Decreases intestinal absorption of glucose
  • Improves insulin sensitivity (increases peripheral glucose uptake and utilization)
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30
Q

What is the effectiveness of Metformin?

A
  • 1st line
  • Lowers A1c by 1.0%, potentially 1.5%
  • Mono-therapy or used w/ any anti-diabetic drugs
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31
Q

What are the CI of metformin?

A
  • Concern for lactic acidosis
  • Kidney disease
  • Acute/unstable HF
  • Drug interactions: Furosemide, anti-HIV, phenytoin, EtOH
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32
Q

What level of GFR do you NOT want to start Metformin? Also, what level of GFR do you need to d/c Metformin in a pt that has been taking it.

A
  • Don’t start: <45 mL/min

- Discontinue: <30 mL/min

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33
Q

What are the ASEs of Metformin?

A
  • Nausea
  • Diarrhea
  • Abdominal cramping
  • Reduce vitamin B12 - megaloblastic anemia is rare
  • Tablets can be malodorous (ER tabs usually less so)
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34
Q

What should you have a pt do to improve GI tolerance to Metformin?

A
  • Take at the end of meal
  • ER formulation
  • Start with 500mg daily or BID then increase
35
Q

What is the MOA of Thiazolidinediones?

A
  • Agonism of PPAR-y receptor located on adipose tissue

- Promotes uptake of circulating fatty acid in fat cells and increases cellular glucose uptake.

36
Q

What is the effectiveness of Thiazolidinediones?

A
  • Highly efficacious

- However, improvement of A1c occurs overtime, weeks to months, 1.0 to 1.5%

37
Q

What is the CI of Thiazolidinediones?

A

Hepatocellular disease in pts with ALT levels >2.5x the normal level
- Monitor liver enzyme

38
Q

What is the ASEs of Thiazolidinediones?

A
  • Water retention and weight gain or increase adiposity
  • Bone density loss
  • Increased fracture risk in women and maybe men
39
Q

Water retention caused by Thiazolidinediones may worsen or cause what?

A
  • May worsen or be confused w/ HF S/Sxs
  • Macular edema
  • Anemia
40
Q

What is a BBW of Thiazolidinediones?

A

May cause of exacerbate CHF

41
Q

What is the MOA of Sulfonylureas?

A
  • Binds to and inhibits sulfonylurea receptor-1 (SUR1)
  • Closes K-channel
  • Leads to B-cell depolarization and insulin exocytosis.
42
Q

What is the effectiveness of Sulfonylureas?

A
  • Variable effectiveness in lowering A1c

- 2nd Gen: 0.5-1.5%

43
Q

What is the CIs of Sulfonylureas?

A
  • Avoid in pts w/sulfa allergies
44
Q

What is the ASE of Sulfonylureas?

A

Hypoglycemia

45
Q

What is the MOA of Glinides (short-acting secretagogues)?

A
  • Closes ATP- senstive K+ channel of pancreatic B cell to stimulate insulin release
46
Q

What is the effectiveness of Glinides (short-acting secretagogues)?

A
  • Shorter acting, give prior to eat meal
  • A1c lowering only 0.5-1.0%
  • No sulfa group
  • Multiple doses 3-4x per day
  • $$$
47
Q

What are the CIs of Glinides (short-acting secretagogues)?

A
  • Do not use w/ insulin of other secretagogues

- If a meal is missed hold dose.

48
Q

What is the MOA of Glucagon-like-peptide (GLP)-1 agonists?

A
  • Stimulates inulin secretion
  • Suppresses post-prandial glucagon secretion
  • Slows gastric emptying
  • Produce an anorectic effect
49
Q

What is the effectiveness of Glucagon-like-peptide (GLP)-1 agonists?

A
  • Works well on reducing serum glucose levels including post-prandial glucose
  • Victoza: 1.0% or more reduction in A1c
  • Decreased risk for MI
50
Q

What is the CI of Glucagon-like-peptide (GLP)-1 agonists?

A

Pts with person or family hx of medullary thyroid carcinoma or in pts with multiple endocrine neoplasia syndrome type 2 (MEN 2)

51
Q

What is the minor ASEs of Glucagon-like-peptide (GLP)-1 agonists?

A
  • Nausea
  • Some weight loss
  • Slows absorption of other orally administered drugs
  • Risk for hypoglycemia when used in combinations w/ insulin or an insulin secretagogues
  • HA
  • Infections
52
Q

What is the serious ASEs of Glucagon-like-peptide (GLP)-1 agonists?

A
  • Pancreatitis
  • Immunological rxns
  • Acute kidney injury
  • Angioedema
53
Q

What is the BBW for Glucagon-like-peptide (GLP)-1 agonists?

A

Thyroid c-cell tumors

54
Q

What is the MOA of Dipeptidyl peptidase (DPP-4) inhibitors?

A
  • Inhibition of dipeptidyl peptidase-4
  • Increases endogenous GLP-1 concentration
  • DPP-4 is a ubiquitous enzyme that metabolize the incretins (ie GLP-1)
55
Q

What is the effectiveness of Dipeptidyl peptidase (DPP)-4 inhibitors?

A
  • Not as effective, 0.5% to 0.8% reduction of A1c.
  • But advantage is that it is oral administration and weight neutral
  • Preferred over GLP-1 by most pts
  • Can be used as monotherapy or w/ metformin to decrease A1c up to 1.5 to 2.0%
56
Q

What is the CI of Dipeptidyl peptidase (DPP)-4 inhibitors?

A

Do not used w/ GLP-1 d/t MOA

57
Q

What is the ASE of Dipeptidyl peptidase (DPP)-4 inhibitors?

A

Risk for Hypoglycemia when used with SU

58
Q

What is the MOA of SGLT-2 inhibitors?

A
  • Low blood glucose by increase urinary excretion of filtered glucose
  • Allows for reabsorption via the sodium glucose co-transporter SGLT

(This transporter can become saturated and that’s what causes glycosuria.)

59
Q

What is the effectiveness of SGLT-2 inhibitors?

A
  • A1c reduction of 1.0%
  • Low risk for hypoglycemia
  • Can reduce systolic BP 3-5 pts
  • Weight loss
  • Reduce CHF and renal events w/ DM2
    (eGFR >30 and estimated urine albumin excretion >300 mg/day)
60
Q

What is the CIs of SGLT-2 inhibitors?

A
  • Severe renal impairments and reduce glucose lowering effect in pts with impaired kidney fxn
  • In women with increased risk for GU infxn
61
Q

What is the ASEs of SGLT-2 inhibitors?

A
  • GU infections: vaginal candidas
  • Diabetic ketoacidosis w/o elevated glucose “Euglycemic DKA”
  • Associated w/ amputation
  • Fournier gangrene
  • Fracture risks
62
Q

What is 1st line tx for DM?

A

Metformin and/or Insulin tx

63
Q

What is 2nd line tx for DM?

A
  • GLP-1 agonist
  • SU
  • DPP-4 inhibitors
  • SGLT-2 inhibitors
64
Q

What is 3rd line tx for DM?

A
  • a-Glucoside inhibitors
  • Bile sequestrants (colesevelam)
  • Thiazolidinediones
  • Bromocriptine
65
Q

What should you start with and when should you consider switching to insulin?

A

Start with oral and switch to insulin if do not meet goal with combination of three or more oral agents

66
Q

What is the ABCDE for tx of DM?

A
  • Abstinence from tobacco
  • B/P (<140/90)
  • Cholesterol (moderate/high-intense statins)
  • Diabetes meds (A1c <7%) and Diet
  • Ecotrin=Aspirin and Exercise
67
Q

What were the issues with Phenformin?

A
  • Higher rates of mortality and lactic acidosis

- Monitor in any pt but CI in pt with kidney disease or acute/unstable heart failure

68
Q

What were the issues with Troglitazone?

A

Rare but severe liver toxicity

69
Q

What were the issues with Rosiglitazone?

A

Myocardial infarction

70
Q

What were the issues with Pioglitazone?

A

Poss. lower liver and MI risks but increased risk of bladder cancer

71
Q

What is the ACC/AHA guidelines that identify how pts w/ DM should be treated with statins?

A

Ages 40-75 should receive moderate intensity statin therapy w/ an option of using high intensity stating therapy for those with > or equal to 7.5% 10 yr ASCVD risk.

72
Q

What is high intensity statin therapy?

A
  • LDL lowering from baseline by 50% or more.
  • Only two statins are capable of this, Rosuvastatin and Atorvastatin (at the very highest dose of 80 mg, but many patients may only be able to tolerate 40 mg
73
Q

What is moderate intensity statin therapy?

A
  • LDL lowering of 30-50%.

- All of the statins (some at the highest doses for the less potent statins) are capable of this degree of LDL lowering.

74
Q

What are pt at risk for when they have both HTN and DM?

A
  • MI
  • CVA
  • Microvascular endpoints
  • Amputation or death from PVD
  • Heart failure
75
Q

What are the best tx options for type 1 and 2 in pts with both HTN and DM?

A
  • Type 1: ACE-inhibitors

- Type 2: ARBs (most evidence) ACE-inhibitors can be used as well)

76
Q

What is the target BP for type 2 pts with both HTN and DM?

A

<140/90 but <130/80 if tolerated and possible

77
Q

What are the two most commonly used antiplatelet drugs used in patients with diabetes?

A
  • Aspirin (usually 81 mg)

- Clopidogrel to reduce risk for CV events in pts with DM

78
Q

What are the names of the 2nd gen Sulfonylureas (“SFUs” or “SUs”)?

A
  • Glipizide
  • Glyburide
  • Glimepiride
79
Q

What are the names of the Non-sulfonylureas/short-acting secretagogues?

A
  • Repaglinide

- Nateglinide.

80
Q

What are the names of the Thiazolidinediones?

A
  • Pioglitazone

- Rosiglitazone.

81
Q

What are the names of the Glucagon-like-peptide-1 agonists (GLP-1)?

A
  • Exenatide
  • Exenatide ER
  • Liragultide (Victorza and Saxenda)
  • Dulaglutide
82
Q

What are the names of the Dipeptidyl-peptidase-4 inhibitors (DPP-4)?

A
  • Sitagliptin
  • Saxagliptin
  • Linagliptin
  • Alogliptin
83
Q

What are the names of the Sodium-glucose transport inhibitors (SGLT-2)?

A
  • Empagliflozin
  • Canagliflozin
  • Dapagliflozin
  • Ertugliflozin
84
Q

When would you use Liragultide (Saxenda)?

A
  • Use as an adjunct to reduce calorie diet and increased physical activity for chronic weight management in adult pts w/ obesity or overweight + weight related comorbidity

Endocrinology (18 decks)

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