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Diabetes Flashcards

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1
Q

Diabetes is the leading cause of what?

A

blindness and ESRD

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2
Q

The effects of insulin

A

promotes glucose removal, glycogen storage, fatty acid storage and protein synthesis, inhibition of ketone body formation in the liver occurs at lower insulin concentrations than that required to stimulate muscle uptake of glucose

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3
Q

postprandial metabolism starts with the release of insulin and results in

A

conversion of glucose to glycogen, conversion of amino acids to protein, conversion of ffa to triglycerides

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4
Q

decreased glucose concentrations causes what

A

shuts off conversion of energy sources to storage, causes release of glucagon, epi, cortisol, growth hormone, glycogenolysis, gluconeogenesis

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5
Q

What are signs and symptoms of diabetes?

A

polyuria, polydipsia, polyphagia, wt loss, fatigue, recurrent UTI, ketoacidosis

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6
Q

Gestational diabetes

A

glucose intolerance during pregnancy, 1-14% of all pregnancies, most common in third trimester, screen conducted three months post partum to test for resolution

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7
Q

Drug induced diabetes

A

antiretrovirals, glucocorticoids, nicotinic acid atypical antipsychotics

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8
Q

Drugs that increase insulin resistance

A

thiazides, niacin

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9
Q

drugs that decrease insulin secretion

A

phenytoin

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10
Q

Drugs that mask S/Sx of hypoglycemia

A

beta blockers

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11
Q

diagnostic criteria for diabetes

A

FPG>126, 2hr GTT >200mg/dL, random plasma glucose >200, A1c>6.5%

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12
Q

How often do you check A1c?

A

every 3 months until at goal and then 6 months

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13
Q

Diagnostic criteria for prediabetes

A

FPG 100-125mg/dL, 2hr plasma glucose 140-199, A1c 5.7-6.4%

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14
Q

Metformin (Glucophage) MOA

A

increases insulin sensitivity, decrease in hepatic glucose production, decreases intestinal absorption of glucose

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15
Q

Metformin dosage

A

500 mg PO BID is starting can increase up to 2000

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16
Q

How much does metformin decrease A1c

A

up to 1-2%

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17
Q

Advantages of metformin

A

no wt gain, no risk for hypoglycemia, decreases risk for micro and macro vascular complications, stroke, MI

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18
Q

Disadvantages of metformin

A

GI side effects, lactic acidosis, contraindicated in renal failure, NYHAIII and IV (CHF), men SCr>1.5, women >1.4

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19
Q

When should metformin be held?

A

temporarily for a few days pre and post any radiographic studies where iodinated contrast is employed

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20
Q

What other disease is metformin used in?

A

polycystic ovarian disease

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21
Q

oral sulfonylureas

A

dlyburide (diabeta), glipizide (glucotrol), glimepiride (Amaryl), glicazide, chlorpromamide, tolazamide, tolbutamide

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22
Q

MOA of sulfonylureas

A

increases insulin secretion from pancreas, may increase insulin sensitivity and reduce glucose production but to a lesser ectent

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23
Q

Sulfonylureas place in therapy

A

first tier option after pt fails metformin and lifestyle modifications, can be used in combination w/ other agents except meglitinides, reduces A1c by 1.5-2%

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24
Q

Advantages of sulfonylureas

A

well tolerated, first tier, old, inexpensive

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25
Disadvantages of sulfonylureas
wt. gain, drug interactions, hypoglycemia
26
Dose of Flimepiride (Amaryl)
2-8mg PO daily
27
Dose of glipizide (Glucotrol)
5-15 mgPO daily, XL
28
dose of glycuride (Diabeta)
5-20 mg PO daily
29
Sulfonylurea pearls
start low, go slow, no value if max exceeded, use with caution with insulin due to increased risk of hypo glycemia, 15% of pts may never respond, 50% fail after 5 years
30
Hypoglycemia symptoms
slurred speech, drowsiness, tachycardia, confusion, agitation, diaphoresis, tremors, coma
31
Treatment of hypoglycemia
goal of 15-30gm carbs, dectrose 50% IVP, glucose tabs, cola, orange juice, hard candy, sugar packets
32
What do you not give for treatment of hypoglycemia
chocolate
33
What is the minimum CNS glucose concentration
40-60 mg/dL
34
How often should you recheck blood glucose after hypoglycemia
15 mins
35
What should be given to a hypoglucose pt who is unconscious
IM glucagon
36
What are the meglitinides
repaglinide (Prandin), Nateglinide (Starlix)
37
MOA of meglitinides
increase in insulin secretion, similar to sulfonylurea but lacks sulfa allergy, faster onset, short duration
38
When should meglitinides be used
in combo with metformin or TZD, not with sulfonylureas because similar MOA, minimal use overall
39
Advantages of meglitinides
accentuated effects around meal ingestion, particularly useful for pts w/ elevated postprandial hyperglycemia
40
Disadvantages of meglitinides
hypoglycemia, poor efficacy, wt gain, dosing frequency (TID), DI
41
When should meglitinides be taken
15-30 mins before a meal, if no meal, skip dose, if add meal, add ose, can adjust dose weekly
42
Thiazolidinedione (TZD)
pioglitazone (actos), rosiglitazone (Avandia)
43
Dose of pioglitazone (actos)
15-45 mg PO daily
44
MOA of TZD
imporves target cell responses to insulin w/out increasing pancreatic insulin secretion, multi-modal MOA
45
What is TZD place in therapy
second tier option after pt fails metformin and lifestyle modifications, combo w/ other agents, reduces A1c by .5-1.4%, take 2-3 months to see full effect
46
Advantages of TZD
no hypoglycemia, increase HDL by 3-9%, decrease triglycerides by 10-20%
47
Disadvantages of TZD
wt. gain, edema, does not decrease LDL, FDA box warning to CHF exacerbation (lifted recently), hepatotoxic
48
Pearls of TZD
not first line, combo w/ OSU, metformin or insulin
49
Incretin physiology
GLP-1: naturally occurring hormone stimulates glucose dependent insulin secretion, dec glucagon release, slows gastric emptying and dec food intake, degrades DPP-4; GIP: inc insulin release, degraded by DPP
50
GLP-1 agonist
exenatide (Byetta), albiglutide (Tanzeum), liraglutide (Victoza), dulaglutide (Trulicity)
51
MOA of GLP-1 receptor agonists
incretin mimetic, inc glucose dependent insulin secretion, dec glucagon secretion, slows gastric emptying, inhibits B cell death
52
Place in therapy of GLP-1 receptor agonists
second tier option for Type 2 DM after pt fails metformin and lifestyle modifications, can be used in combo w/ other agents
53
Advantages of GLP-1 receptor agonist
wt reduction, potential for improved B cell function
54
Disadvantages of GLP-1 receptor agonist
GI- N/V/D, cases of acute pancreatitis reported, long term safety unknown, injectable (sq BID)
55
Dose of exenatide (Byetta)
5-10 mcg sub cut BID, extended release 2 mg weekly
56
Dose of liraglutide (Victoza)
.6-3 mg subcut daily
57
Dipeptidyl peptidase inhibitors
Sitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta), alogliptin (Nesina)
58
Dose of sitagliptin (Januvia)
50-100 mg PO daily, adjust renal
59
Dose Saxagliptin (Onglyza)
2.5-5 mg PO once daily
60
Dose of Linagliptin (Tradjenta)
5 mg PO daily
61
DPP-4 inhibitors MOA
inhibits DPP-4 activity which prolongs the survival of endogenously release incretin hormones, results in greater GLP-1 concentrations
62
Place of DPP-4 inhibitors in therapy
may be used as monotherapy or in combo with OSU, metformin, TZD, or insulin, may be first line eventually
63
DPP-4 inhibitors advantages
no hypoglycemia, PO, wt neutrality, well tolerated
64
Disadvantages of DPP-4 inhibitors
cases of angioedema, acute pancreatitis observed, long term safety unknown, $$, $200/ month
65
Sodium glucose costransporter 2 inhibitors
Canagliflozin (Invokana), dapagliflozin (Farxiga), empagliflozin (jardiance)
66
MOA of SGLT2 inhibitors
work to reduce reabsorption of filtered glucose from the tubular lumen in proximal renal tubules. lower renal threshold for glucose
67
place in therapy of SGLT2 inhibitors
new products, no established recommendations, FDA approved for type II, monotherapy
68
Advantages of SGLT2 inhibitors
already available in combo w/ metformin, oral, once daily formulation, novel MOA, quick onset, dec A1c by .7-1%, efficacy best if taken in am
69
Disadvantages of SGLT2 inhiitors
avoid CrCl
70
a-Glucosidase inhibitors
acarbose (Precose), miglitol (glyset)
71
MOA of a Glucosidase inhibitors
inhibits intestinal a glucosidase resulting in slowed carbohydrate digestion and absorption
72
Place in therapy for a glucosidase inhibitors
as adjunct with other agents for post prandial hyperglycemia, .4-1% A1c reduction
73
advantages of a-glucosidase inhibitors
no systemic effects, no wt gain, specific for post-prandial hyperglycemia
74
Disadvantages of a-glucosidase inhibitors
GI, flatulence is sig, diarrhea, dosing frequency, bad if pt on low carb

Pharmacology (61 decks)

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