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ENRP Exam 2 > Drugs For Diabetes Dr. Konorev > Flashcards

Drugs For Diabetes Dr. Konorev Flashcards

1
Q

Insulin activates what 2 things

A

Glycolysis + Glycogen synthase

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2
Q

2 drug classes that can treat T1D

A

Insulins + Amylin Analog

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3
Q

Rapid Acting Insulins

  1. 3 of them
  2. Clinical use + administration
  3. Duration
A
  1. Aspart, Lispro, Glulisine
  2. Postprandial hyperglycemia (Take before meal, IV)
  3. 1hr-3hr
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4
Q

Short Acting Insulins

  1. 1 of them
  2. Clinical use + administration
  3. Duration
A
  1. Regular Insulin
  2. Base insulin regulation + Postprandial hyperglycemia (IV 45min before meal) + Overnight coverage
  3. 3hr-5hr
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5
Q

Intermediate Acting Insulins

  1. 1 of them
  2. Clinical use + administration
  3. Duration
A
  1. NPH (Neutral Protamine Hagerdorn) use is declining = protamine + Zn insulin
  2. Maintenance + overnight
  3. 10hr-12hr
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6
Q

Long Acting Insulins

  1. 2 of them
  2. Clinical use + administration
  3. Duration
A
  1. Detemir (Lys 29, rapid absorption + binds to albumin) + Glargine (low pH solvable insulin)
  2. Maintenance + overnight
  3. 24hr, inject 1-2 times a day
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7
Q

Insulin is used also in what besides DM

A

Hyperkalemia sever, (Insulin + glucose) = takes long time

Loop Diuretics also given for immediate elimination of K+

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8
Q

Artificial or bionic pancreas

A

Insulin delivery system )glucose sensor + microchip controlling + insulin pump
= NON invasive, placed over BVs on skin to measure blood glucose with electromagnetic waves

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9
Q

Adverse effects insulin

A
  1. Hypoglycemia
  2. Lipodystrophy : hypertrophy of SubQ fat at injection site
  3. IgG against insulin = resistance
  4. Allergic reaction rare
  5. Hypokalemia*
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10
Q

Hypoglycemia is usually caused with during insulin tx

A
  1. Delay of meals or missed meal
  2. Exercises
  3. Insulin overdose
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11
Q

Hypoglycemia SX

A
  1. CNS, confusion, coma,
  2. Tachy, sweating, tremor, palpitations, hunger, N,
    TX = give glucagon or sucrose/glucose
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12
Q

Amylin Analog

  1. What is it
  2. MOA
A
  1. Pancreatic H made by B-cells
  2. Enhance insulin action by (inhibiting glucagon secretion, lower gastric emptying for more absorption time, increase satiety)
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13
Q

Amylin Analog:

  1. 1 drug
  2. Clinical use
  3. Duration
A
  1. Parmlintide SUB Q* administration
  2. T1D**, T2D with mealtime insulin, (injected with insulin before meals when there is no insulin in the pt)
  3. 3hr
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14
Q

Pramlintide side effects

A
  1. N, V, Hypoglycemia, Constipation
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15
Q

Glucose to insulin release happens how

A
  1. Glucose binds GLUT 4
  2. K+ channel closes = increases ATP
  3. Depolarization happens
  4. Ca+ goes into cell (when PKA is phosphorylation)
  5. Insulin leaves cell
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16
Q

Drug types increasing Gs (more insulin) and drugs increasing Gi (lowerring insulin)

A
  1. Gs: B2 agonist (isoproterenol) + GLP-1 agonist (incretin)
  2. Gi : Somatostatin + a2 agonist + B Blockers
17
Q

GLP-1 role and and reason it is not as useful

A
  1. Increase insulin, lower glucagon, B-cell proliferation

2. Very short half-life (1-2min) due to DPP-4 cleaving it

18
Q

Incretin drugs that are useful

A
  1. Long-Acting GLP1 receptor agonist

2. DPP-4 inhibitors (keeps GLP-1 from being cleaved)

19
Q

Long-Acting GLP1 receptor agonist

  1. 2 drugs
  2. Clinical use
A
  1. Exenatide (from Gila monster saliva 2.4hr) + Lirglutide (binds to albumin 11-15hr)
  2. T2D patients that are not adequately controlled by metformin , Sulfonylurea, Thiazolidinediones + oral drug
20
Q

Long-Acting GLP1 receptor agonist SIDE EFFECTS

A

Hypoglycemia (lower then insulin + Sulfonylurea) , N,V, D

21
Q

DPP4 inhibitors

  1. 4 Drugs
  2. MOA
  3. Clinical use
A
  1. Sitagliptin, Linagliptin, Saxagliptin, Alogliptin
  2. Increase GLP levels due to not cleaving it
  3. Adjunct to diet and exercise in T2D, can be taken with metformin and he other drugs
22
Q

Sulfonylureas :

  1. 1st gen drugs
  2. 2nd gen drugs
  3. 2 nonsulfonylureas drugs (Meglitinides)
A
  1. Chlorpropamide + Tolbutamide + Tolazamide
  2. Glipizide + Glyburide + Glimepiride
  3. Nateglinide + Repaglinide
23
Q

Sulfonylureas :

  1. MOA
  2. Half-life
  3. Clinical use
A
  1. K ATP channel Blockers (bind to SUR1. +Kir6.2 to block)

2. T2D main drug , Meglitinides are short (before eating)

24
Q

Sulfonylureas 1st gen

A

Infrequent use , ,used in high doses

25
Q

Sulfonylureas 2nd gen

A 
Higher potency (lower dose) , lower adverse effects
= used more
26
Q

Sulfonylureas side effects

A
  1. Hypoglycemia**

2. Increased weight gain from insulin increase *

27
Q

Sulfonylureas drug interactions *

A
  1. NSAIDS, alcohol, anti-fungal = enhance hypoglycemia

2. B-blockers, CCB, hepatic CYP enzymes = increase glucose in blood lower Sulfonylureas effectiveness

28
Q

Meglitinides

  1. MOA
  2. Clinical use
A
  1. K + blocker (similar to Sulfonylurea)

2. Short half-life, so before eating

29
Q

METFORMIN

  1. MOA
  2. Clinical use
  3. Advantages
A
  1. AMP-activated protein kinase activator (increase ATP uptake processes and decrease ATP consumption) = lowering glucose
  2. 1st line for T2D, oral (purpose to get glucose levels and A1C levels right)
  3. Does not cause hypoglycemia, does not cause weight gain, decrease macro and micro vascular complications in DM
30
Q

METFORMIN

  1. Half-life
  2. Adverse effects
A
  1. 1.5hr-3hr (no drug-drug interactions)
  2. = GI N,D, ABD pain
    = Lactic acidosis (esp if renal or hepatic insufficiency)
    = contraindications in HF, COPD, renal failure, chronic alcoholism, cirrhosis (tissue hypoxia)
31
Q

Thiazolidinediones

  1. 2 drugs
  2. MOA
A
  1. Pioglitazone + Rosiglitazone

2. PPAR-gamma nuclear R in muscle, liver, fat, endothelium (activated cause peroxisome proliferations) = INCREASE GLUT4

32
Q

Thiazolidinediones

  1. Administration
  2. Clinical use
  3. Adverse effects
A
  1. Oral, full effect after 1-3mo
  2. Safe in pt what renal insufficiency + T2D, DELAYS PRE-DM to DM + no hypoglycemia (makes insulin for sensitive, lowering resistance)
  3. Weight gain, edema (increased vascular permeability, increase NA and water reabsorption =edema, CONTRAindicated in HF) + suppress MSCs into osteoblasts = osteoporosis esp in women
33
Q

Euglycemic drugs (does not cause hypoglycemia) however lower blood glucose to normal level

A

Thiazolidinediones + Metformin (not insulin and K+ blockers)

34
Q

Gliflozins :

  1. MOA
  2. 3 drugs
A
  1. Na+/Glucose cotransporter 2 inhibitor (SGLT2 inhibitors) = reduce reabsorption of glucose in Proximal Tubule
  2. Canagliflozin+ Dapagliflozin + Empagliflozin
35
Q

Gliflozins

  1. Clinical use
  2. Adverse effects
A
  1. NEW drug, no hypoglycemia, T2D lower glucose in blood , REDUCE BP (improve Cardiac and renal problems and future probs) orally before 1st meal
  2. WL, lower uric acid, osmotic diuresis (dehydration)
36
Q

Gliflozins contraindications in and serous adverse effects

A
  1. Hypotension

2. Hypovolemia (orthostatic hypotension, dizziness, syncope) + UTI, genital infection

37
Q

A-glycosides inhibitors

  1. 2 drugs
  2. MOA
  3. Clinical use
A
  1. Acarbose + Miglitol
  2. Inhibit GI absorption of glucose to blood
  3. Lower postprandila hyperglycemia ( you dont need that much insulin)
38
Q

A-glycosidase inhibtors

  1. Advantages
  2. Adverse effects
A
  1. No hypoglycemia, no WG, T2D before meals

2. Malabsorption, d, flatulence, bloating

ENRP Exam 2 (8 decks)

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