Chapter 13: Diabetes Flashcards

(119 cards)

1
Q

Type 1 DM

A

2-5% of all cases

induced by auto-immune destruction of pacnreatic cells

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2
Q

Type 2 DM

A

90-95% of cases

prevalence varies by ethnicity

strong genetic predisposistion

plasma insulin levels drop as the body develops resistance

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3
Q

oral hypoglycemics

A

sulfonylureas

biquanides

alpha-glucosidase inhibitors

thiazolidines

meglitinides

DPP-4 inhibitors

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4
Q

glucosuria

A

glucose in urine d/t kidney excreting too much

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5
Q

polyuria

A

increased urination

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6
Q

polyphasia

A

increased appetitie

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7
Q

polydipsia

A

increased thirst

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8
Q

poor glycemic control places at a high risk for

A

retinopathy

neuropathy

MI

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9
Q

what is treatment for T2DM based on

A

HGBA1C results

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10
Q

what medications are obese patients more likely to benefit from and why

A

metformin because it acts more on glucose utilization and hepatic glucose storage and production

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11
Q

which medication do non-obese diabetic patients respond better to

A

sulfonylureas

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12
Q

patients who are at risk for hypoglycemia benefit more from which drug and why

A

metformin because it is less likely to produce it

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13
Q

what do patients with a high postprsndial glucose level beneit most from

A

addition of a glucosidase inhibitor or a meglinitidine

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14
Q

steps for treatment of T2DM

A
  1. lifestyle intervention and metformin (titrated to maximum effective dose over 1-2 months)
  2. additional medications
  3. glycemic control (start insulin)
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15
Q

sulfonylureas

mechanism of action

A
  • lowers blood glucose by increasing insulin secretion from pancreatic Bcell
  • decreases glycogenolysis
  • decreases glyconeogenesis
  • increase cell sensitivity to insulin
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16
Q

sulfonylureas clinical uses

A

monotherapy an in combination with other drug classes as well as insulin

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17
Q

sulfonylureas should not be used in combination with what

A

meglitinides

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18
Q

why is there controversy ove whether sulfonylureas should be as first line therapy for T2DM

A

only lowers A1C levels by 1-2%

1st class of drugs used to treat T2DM

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19
Q

conscientious prescribing of sulfonylureas

A

start low, go slow, watch for toxicity

mild-mod T2DM responds best

combination therapy is popular

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20
Q

the only sulfonylureas that doe not cause weight gain

A

metformin

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21
Q

patient education for sulfonylureas

A

take 30-40 minutes before eating and never on an empty stomach

watch for weight gain, GI upset, gas

avoid alcohol and ASA

accu-checks

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22
Q

what medications increase the effects of sulfonylureas

A

CYP450 inhibitors

(azoles, NSAIDs, sulfonamides, antidepressants, MAOIs, and digitalis)

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23
Q

what medications may decrease the effects of sulfonylureas

A

CYP450 inducers

(phenobarbital, beta blockers, and hydantoins)

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24
Q

sulfonylureas contraindications

A

cross-sensitivy to sulfonamides (including thiazide diuretics)

severe renal, hepatic, thyroid, or other endocrine disorders

uncontrolled infection, burns, and trauma

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25
biguanides: Metformin (Glucophage)
first line therapy lowers A1C 1-2%
26
metformin mechanism of action
reduces hepatic production of glucose and inhibits intestinal absorption of glucose
27
metformin clinical uses
monotherapy and in combination with other agents
28
conscientious considerations for metformin
* decreases LDL, trigs, plasminogen, B12 * combinations are more effective than monotherapy * monitor renal function for ketoacidosis * dc if hypoxic or surgery * assess for HF, septicemia metabolic acidosis, pregnancy * many drug interactions
29
patient education for metformin
take missed dose within an hour of scheduled dose or waite until next scheduled dose healthy diet, avoid alcohol regular follow-up is necessary test for blood glucose and urine ketones
30
what medications may increase metformin levels
lasix, nifedipine, cimetidine, cationic drugs (digoxin, amiloride, procainamide, quinidine, ranitidine, trimethoprim, vancomycin, triamterene, morphine)
31
what medications increase hyperglycemia risk when taken with metformin
thiazides and other diuretics, corticosteroids, phenothiazines, thyroid products, estrogens, oral contraceptives, phenytoin, nicotinic acid, sympathomimetics, CCBs, and isoniazid
32
what can cause hypoglycemia when taken with metformin
alcohol excess alcohol can increase risk for lactic acidosis
33
metformin contraindications
those at increased risk for lactic acidosis d/t renal impairment hepatic dysfunction, HF, metabolic acidosis, dehydration, alcoholism
34
Meglitinides: secretagogues mechanism of action
close ATP-dependent potassium channels in the beta cell membrane by binding at specific receptor sites causing insulin release lowers A1C by 0.6-1%
35
examples of meglitinides
repaglinide (Prandin) nateglinide (Starlix)
36
why must meglitinides be adminstered more often than sulfonylureas
they have a shorter half-life
37
meglitinides clinical usage
postprandial hyperglycemia
38
which meglitinide is almost as effective as metformin
repaglinide
39
meglitinide dosages are based on
A1C levels
40
meglitinide therapy
monotherapy has better long term effects may need adjunct insulin in times of stress
41
what medications may lead to increased serum concentrations of meglitinides resulting in hypoglycemia
gemfibrozil, macrolide antibiotics, many herbals (St. John's wort, ethanol, garlic), any drug affected by the CYP450 system
42
meglitinides contraindications
hepatic impairment
43
meglitinide patient education
take with meals 2-4 times a day watch for weight gain and hypoglycemia
44
thiazolidinediones (TZDs) mechanism of action
increase sensitivity of muscle, fat, and liver to endogenous and exogenous insulin improves cellular response to insulin without increasing output of insulin from the pancreas
45
benefits of TZDs
do not produce hypoglycemia in diabetic or nondiabetic patients
46
most common adverse effects of TZDs
weight gain, fluid retention
47
clinical use of TZD
indicated as monotherapy and in combination with metformin, sulfonylureas, and insulin
48
TZD patient education
increased risk for HF
49
what should be monitored when on TZDs
LFTs (closely for 1st year d/t risk of hepatotoxicity) edema, cytopenia HDL, trigs
50
TZDs with oral contraceptives
ovulation may resume
51
TZD medication interactions
phenobarbital, amiodarone, rifampim, fluconazole, medications metabolized by CYP450 system (carbamazepine, cyclosporine, felodipine, and some oral contraceptives)
52
TZD contraindications
CHF hepatic impairment
53
alpha-glucosidase inhibitors mechanism of action
reduce rate of digestion of polysaccharides in the proximal small intestine by lowering postpradnial glucose levels without causing hypoglycemia (reduces A1C by approx 1%)
54
common side effects of alpha-glucosidase inhibitors
increased gas and GI symptoms
55
examples of alpha-glucosidase inhibitors
acarbose miglitol
56
alpha-glucosidase inhibitors as monotherapy
seldom gives satisfactory results
57
conscientious prescribing for alpha-glucosidase inhibitors
start low, go slow increase dose slowly over several weeks in increments of 2.5mg to minimize GI upset
58
Patients who show signs of hypoglycemia while being treated with alph-glucosidase inhibitors
treat with glucose not sucrose
59
why is periodic LFTs indicated with acarbose
has been associated with raised liver enzymes
60
what should be monitored for with alpha-glucosidase inhibitor therapy GI/GU
diabetic ketoacidosis, IBD, colonic ulceration, partial intestinal obstruction, chronic intestinal disease, renal function, pregnancy statius
61
is insulin needed with alpha-glucosidase inhibitor therapy
occasionally adjunct in time of stress
62
alpha-glucosidase inhibitor patient education
diet/exercise side effects follow-up dosage may need adjustment during stress
63
miglitol interactions
may decrease absorption of digoxin, propranolol, and ranitidine
64
acarbose interactions
may decrease effects of digoxin, thiazide diuretics, thyroids, estrogens, oral contraceptives, and CCBs
65
alpha-glucosidase inhibitor contraindications
IBD GI obstruction colonic ulceration cirrhosis malabsorption syndrome
66
what is the only drug in the amylin analogue class and what is its make-up
pramlintide (Symlin) synthetic analogue of human amylin
67
amylin analogue mechanism of action
neuroendocrine action that regulates glucose influx, including glucagon suppression, slowing of gastric emptying, and a potential effect on feeding behavior and weight control
68
clinical uses for amylin analogue
adjunct treatment in patient with either type DM who have not achieved desired insulin control despite optimal insulin therapy with or without sulfonylureas and/or metformin in T2DM
69
amylin analogue conscientious prescribing
adjust dose after owering insulin dose
70
what tests are used to assess health in patients taking amylin analogues
FPG, HGBA1C, renal function, LFT, CBC
71
what should be adusted prior to begining therapy with amylin analogues
reduce insulin dose by 50% and monitor BG frequently
72
amylin analogue patient education
carry fast-acting sugar at all times DO NOT mix with insulin (sepatate injections) administer immediately prior to major meals should be able to reduce insulin dose by 1/2 will need to frequently monitor BG
73
black box warning for amylin analogue
use with insulin insulin induced severe hypoglycemia can occur within 3 hours of injection
74
amylin analogue interactions
do not administer with medications that alter GI motility or slow intestinal absorption (anticholinergic agents like atropine or alpha-glucosidase inhibitors)
75
amylin analogue and analgesics
administer analgesics and other oral agents that require rapid onset 1 hour before or 2 hours after injection
76
amylin analogue contraindications
hypoglycemia unawareness gastroparesis
77
glucagon-like peptide-1 (GLP-1) agonists drug namess
exenatide (Byetta)
78
GLP-1 agonists mechanism of action
analogue of the hormone incretin, which increases insulin secretion high frequency of GI side effects
79
clinical uses of GLP-1 agonists
combination therapy only for patients with T2DM that have not achieved glycemic control using metformin, a sulfonylurea, or both
80
byetta conscientious prescribing
not a substitute for insulin monitor for pancreatitis assess for T1DM, renal function, GI-paresis, HGBA1C
81
GLP-1 agonists patient education
take within 60 of morning and evening meal if dose missed resume treatment at next dose report side effects keep drug away from light discard pen after 30 days of first use
82
GLP-1 agonists and warfarin
may increase INR and cause bleeding
83
GLP-1 agonists interactions
drugs dependant on threshold concentrations for efficacy (contraceptives, antibiotics) should be taken 1 hour before caution with drugs that require rapid GI absorption
84
GLP-1 agonists contraindications
T1DM treatment of diabetic ketoacidosis severe renal impairment severe GI disease
85
dipeptidyl-peptidase-4 inhibitors (DDP-IV) mechanism of action
slows the inactivation of incretin hormones (GLP-1 and gluosce-dependent insulinotropic polypeptide) intestinal concentrations of these are decreased in T2DM
86
DDP-IV clinical uses
approved as monotherapy or in combination with metformin or thiazolidinedione
87
DDP-IV (Januvia) conscientious prescribing
may experience weight loss watch for skin conditions (Steven's Johnson syndrome) test for renal function, FPG, HGBA1C, hypoglycemia
88
DDP-IV patient education
adjunct to diet and exercise counsel about adverse effects (nasopharyngitis, headache, URIs) advise dosing may need adjusted during stress
89
examples of DDP-IV
sitagliptin (Januvia) saxagliptin (Onglyza) saxagliptin/metformin (Kombiglyze) sitagliptin/metformin (Janumet)
90
DDP-IV interactions
may increase digoxin levels may require lower dose of sulfonylurea to reduce risk of hypoglycemia
91
DDP-IV contraindications
anaphylaxis angioedema
92
glucagon mechanism of action
increases BG levels
93
glucagon clinical uses
treat severe hypoglycemia diagnstic aid for radiologic exam of the stomach, duodenum, small bowel, colon
94
when is glucagon not effective
states of starvation, adrenal insufficiency, chronic hypoglycemia, insufficient liver glycogen
95
glucagon contraindication
pheochromocytoma
96
what is the oldest available medication to treat T1DM
injectable insulins
97
what are injectable insulins ade from
derived from beef or prok or synthesized using recombinant DNA technology using strands of E. Coli
98
four categories of injectable insulins
regular protamines lentes modifieds
99
insulin for special populations
used for gestational diabetes less stringent glycemic control set for elderly children should be referred to pediatric endocrinologist if multiple drugs are needed
100
why are glycemic controls less stringent for elderly
increased risk for hypotension and long-term microvascular complications
101
types of insulins
rapid acting short acting intermediate acting long acting
102
examples of rapid acting insulins
aspart (Novolog) lispro (Humalog)
103
examples of short acting insulins
regular insulin (Humalog-R, Humalin-R)
104
examples of intermediate acting insulins
NPH insulin zinc (Humulin N) lente isophane insulin suspension
105
examples of long acting insulins
insuline glargine (Lantus) insulin detmir (Levimir) extended zinc (UltraLente) protomine zinc (PZ)
106
injectable insulins conscientious prescribing
have a plan for starting/maintainingg dosages may need higher doses for T2DM dosage adjustments should be step-wie change regimen if goals not met in 2-3 days can change from rapid to long acting at largest meal of the day
107
injectable insulin patient education
measure BG at least twice daily
108
effect of insulin on glucose cell membrane
acts on the membranes transporters that regulate insulin release and glucose homeostasis
109
why is it so hard to induce weight loss as part of a diabetes management regien
total number of insulin receptors acan be downregulated by obesity
110
insulin and liver
where glucose increases storage of glucose as glycogen and resets the liver;s catabolic activity after ingesting food
111
insulin and adipose tissue
where insulin reduces circulating free fatty acids and promotes storage of triglycerides in adipose tissue
112
insulin and muscle cell growth
where insulin promotes protein synthesis by increasing amino acid activity and glycogen synthesis to replace glycogen that has been depleted during work or exercise
113
general rule of insulin dosing
0.6-1 unit per kilogram of body weight
114
lente insulins
modified by a fish protein which prolongs insulin action
115
protamine insulin
modified by zinc moiety which prolongs insulin action
116
symptoms of diabetic ketoacidosis (DKA)
drowsiness, dim vision, and labored breathing preceded by a lengthy episode of polyuria, polydipsia, polyphagia, weight loss, vomiting, dehydration, and ketone odor to breath
117
what is DKA usually the result of
undue stress, illness, infection, missed insulin
118
treatment of DKA
requires hospitalization and correction of acid/base, fluid, and glucose imbalances
119
drugs that interact with insulin
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