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DM Flashcards

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1
Q

What are the different types of diabetes

A
  1. Type 1: Juvenile onset ( IDDM) - childhood/puberty
  2. Type 1.5: LADA (Latent Autoimmune Diabetes of Adults) - Adults
  3. Type II: Maturity onset (NIDDM) - >35 years of age
  4. MODY (Maturity onset diabetes of the young) - 20-60 years of age
  5. Gestational - pregnant women
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2
Q

What is the prevalence of diabetes

A

9.3%

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3
Q

Which type of diabetes include autoantibodies that target B cells of the pancreas responsible for insulin production

A
  1. Type 1

2. LADA

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4
Q

in which type of diabetes is one considered undernourished

A

type 1

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5
Q

in which type of diabetes is one considered obese

A

type II

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6
Q

in which type of diabetes do you see insulin resistance

A

type 1, LADA (some)

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7
Q

in which type of diabetes do you see a genetic predisposition

A
  1. type I (polygenic and environmental)
  2. type II (polygenic and environmental)
  3. MODY (autosomal dominant–> monogenic)
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8
Q

What is the defect of deficiency of each type of diabetes?

A
  1. type I: Beta cells are destroyed
  2. LADA: slow progression to insulin dependence
  3. type II: inability of beta cells to produce adequate insulin
  4. MODY: defective insulin production or secretion
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9
Q

What are the classic symptoms of diabetes? (three P’s)

A
  1. polydipsia (always thirsty)
  2. polyuria (always urinating)
  3. polyphagia (always eating)

(signs include high blood sugar)

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10
Q

Therapy of diabetes include keeping A1-C below _____blood pressure below ____ and LDL cholesterol below ____

A

7.0; 140/80; 100

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11
Q

____% of diabetics are type 1

A

5

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12
Q

what does glycosylated hemoglobin bind to

A

red blood cells; the higher the levels of A1C, the higher the presumed glucose levels

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13
Q

what are normal glucose levels

A

70-110 mg/dl

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14
Q

what is the formula to determine eAG (estimated average glucose)

A

28.7 x A1C - 46.7

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15
Q

what does it mean when a patient tells you their A1C is 7?

A

That their average blood sugar is around 150

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16
Q

what are the diabetic drug classes

A
  1. oral hypoglycemics

2. injectable hypoglycemics (insulin and GLP- 1 agonists)

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17
Q

what are the oral hypoglycemic therapeutics

A
  1. biguanides
  2. sulfonylureas
  3. thiazolidinediones/glitazones
  4. DPP- 4 inhibitors
  5. SGLT 2 inhibitors
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18
Q

what is at the top of initial drug therapy for treating type II diabetic patients

A

metformin; efficacy in reducing hemoglobin A1 is high, and low risk for hypoglycemia

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19
Q

when do we prescribe insulin for diabetic patients? what is one of the key factors that is recognized in taking insulin?

A

when all else fails (tried mono therapy, two drug combinations and three drug combinations). key factor is weight gain.

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20
Q

what are the 3 classes of hypoglycemic agents that do not produce weight gain

A
  1. biguanides (metformin)
  2. DPP - 4 inhibitors
  3. GLP - 1 agonists
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21
Q

what is the trade name of metformin

A

glucophage

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22
Q

what is the indication for metformin

A
  1. diabetes mellitus type II

2. polycystic ovary syndroma (taken for infertility)

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23
Q

what is the MOA of metformin

A

Activates AMP activated protein kinase (AMPK) which in turn suppresses hepatic gluconeiogenesis and intestinal glucose absorption; increases insulin sensitivity.

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24
Q

what are AE of metformin

A
  1. headache
  2. metallic taste
  3. rash
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25
what are serious AE of metformin
1. lactic acidosis | 2. megaloblastic anemia
26
which drugs/supplements increase blood sugar while taking metformin
fish oils and decongestants
27
while on metformin which drug/supplement causes a decrease in metformin
flaxseed
28
while on metformin, which drugs cause nephrotoxicity and induce lactic acidosis
1. aminoglycosides 2. amphotericin 3. gancyclovir 4. acyclovir
29
which drug masks hypoglycemia
beta blockers
30
T/F beta 2 causes gluconeogenesis and increased insulin relase
True
31
T/F alpha 2 causes decreased insulin release
true
32
which sulfonylureas have a greater potency...first generation or second generation?
second generation
33
what are the second generation sulfonylureas
1. glipizide | 2. glibenclamide
34
what is the indication for glipizide
DM type II
35
what is the MOA of glipizide
1. stimulates pancreatic islet beta cell insulin release. 2. actions involve binding to an ATP dependent K+ channel; blocked efflux leads to depolarization, Ca++ release and insulin vesicle effusion.
36
what are common AE of glipizide
1. headache 2. photosensitivity 3. hypoglycemia
37
what are serious AE of glipizide
death
38
what are drug interactions of glipizide
1. decongestants (antagonistic) 2. steroids (antagonistic) 3. flax seed oil (additive) 4. fluoroquinolones (unpredictable) 5. NSAIDS (prolonged effects)
39
T/F thiazolidinediones (TZD) are termed for their structural/molecular reference
True
40
what are the two TZDs
1. Pioglitazone (actos) | 2. Rosiglitazone (avandia)
41
what is the indication for pioglitazone
Diabetes mellitius type II
42
what is the MOA of Pioglitazone
A thiazolidinedione insulin sensitizer selectively stimulates nuclear receptor PPAR (peroxisome proliferator activated receptor) which increases insulin sensitivity in liver, skeletal muscle and adipose tissue.
43
when we talk about PPAR which subtype are we talking about?
gamma--> leads to transcription of certain substances that sensitize the body to insulin. Takes lipids out of circulation so that the body makes more use of the glucose.
44
what are common AE of pioglitazone
1. fluid retention 2. weight gain 3. headache 4. sinusitis 5. pharyngitis 6. dyspnea
45
what are serious AE of pioglitazone
1. diabetic macular edema | 2. bladder cancer
46
what are drug interactions of pioglitazone
1. decongestants, corticosteroids, and sympathomimetics (antagonistic) --> dump sugar into bloodstream 2. flaxseed (additive) 3. beta blockers (mask hypoglycemia) 4. azoles, trimethoprim (impaired metabolism)
47
which drug is a common DPP-4 inhibitor which does not cause weight gain
Sitagliptin
48
what is the MOA of sitagliptin
inhibits dipeptidyl peptidase 4, slowing incretin (GI hormones normally released during a meal) breakdown, increasing insulin synthesis/release, decreasing glucagon levels.
49
what are common AE of sitagliptin
headache
50
what are serious AE of sitagliptin
1. renal failure | 2. SJS
51
What is a common SGLT-2 inhibitor
Canagliflozin
52
what is the MOA of canagliflozin
inhibits sodium glucose cotransporter 2, reducing glucose reabsorption and increasing urinary glucose secretion.
53
what are common AE of canagliflizon
increased urination, thirst, and dehyrdation
54
what are serious AE of canagliflozin
1. orthostatic hypotension | 2. fractures, bone density loss--> we are losing calcium which is a key electrolyte responsible for bone mass.
55
Fluoroquinolones cause additive _____ while taken with canagliflozin
hypoglycemia
56
Dulaglutide is a _____ agonist which gets injected once a week for DM type II
GLP-1 agonist
57
what is the MOA of dulaglutide
activates glucagon like peptide-1 (GLP-1) receptor on beta cells, increasing insulin secretion, decreasing glucagon secretion, and delaying gastric emptying (incretin mimetic).
58
what are common AE of dulaglutide
tachycardia
59
what are serious AE of dulaglutide
1. hypersensitivity | 2. thyroid carcinoma
60
what are insulin based therapies that are long acting basal analogues
1. insulin glargine (lantus) #6 highest selling drug in America! 2. insulin detemir (levemir)
61
what are advantage of insulin
1. universally effective 2. unlimited efficacy 3. decreased microvascular risk
62
What are disadvantage of insulin
1. hypoglycemia 2. weight gain 3. mitogenicity: cell replication. 4. injected 5. training requirements 6. "stigma"
63
what are the rapid acting insulin?
1. lispro 2. aspart 3. glulisine
64
what are the intermediate acting insulin
NPH
65
what are the long acting insulin
1. glargine | 2. detemir
66
what is the MOA of insulin glargine
slow release, micro- crystalized rDNA insulin analog for stable day long blood sugar regulation to be used in post prandial combination with fast acting insulin.
67
what are common AE of insulin glargine
1. hypoglycemia 2. local lipo-dystrophy 3. pruritus 4. weight gain 5. edema
68
when are you supposed to caution with use of insulin glargine
infection --> glucose is dumped into bloodstream, and blood becomes viscous. That viscosity impairs the mobility of immune cells that have been mobilized to fight the infection. So when a diabetic gets an infection and if they have poor blood sugar regulation, they will be more prone to complications from that infection due to high glucose in the bloodstream.

Systemic Pharm (9 decks)

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