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Block 10 Week 2 > Insulin and Oral hypoglycemics- Duan > Flashcards

Insulin and Oral hypoglycemics- Duan Flashcards

1
Q

In healthy humans, blood glucose is tightly maintained (normal fasting blood sugar level is (blank) mg/dL, two hours after eating is (blank) despite wide fluctuations in glucose consumption, utilization, and production.

A

70-99

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2
Q

Adjusting the amount of insulin secreted from the (blank) cell is central in the glucose homeostasis process.

A

pancreatic β

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3
Q

The islet cells in the endocrine pancreas comprise (blank) percent of pancreatic volume.
These cells are highly (blank, blank) and contain multiple cell types secreting a variety of hormones

A

1-2%
vascularized
innervated

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4
Q

What do alpha cells (make up 20% of islet mass) of the pancreas secrete?

A

glucagon

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5
Q

What do beta cells (make up 75% of islet mass) of the pancreas secrete?

A

insulin, C-peptide, amylin

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6
Q

What do pancreatic D cells secrete?
E cells?
G cells?
G cells (PP Cells)?

A

somatostatin
ghrelin
gastrin
pancreatic polypeptide (PP)

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7
Q

What is the standard preparation for insulin?

A

Humulin (human insulin preparations, recombinant protein)

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8
Q

How do you treat Diabetes?

A

insulin
hypoglycemics
oral agents
non-insulin injectables

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9
Q

What are the 6 types of oral hypoglycemics?

A

1) insulin secretagogues
2) insulin sensitizers
3) a-glycosides
4) Dipeptidyl peptidase 4
5) GLucagon like peptide analogue
6) sodium glucose cotransporter 2 (SGLT2)

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10
Q

What are the insulin secretagogues?

A 
sulfonylureas
-tolbutamide
-chlorpropamide
-glipizide
-glyburide
Non sulfonylurea
-meglitinides
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11
Q

What are the insulin sensitizers?

A 
Biguanides
-metformin
Thiazolidinediones (TZD)
-Rosiglitazone
-Pioglitazone
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12
Q

What are the alpha-glycosidase inhibitors (AGI)?

A

acarbose

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13
Q

What are the dipeptidyl peptidase 4 (DPP-4) inhibitors?

A

sitagliptin

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14
Q

What are the Glucagon like peptide (GLP-1) analgogues?

A

exenatide

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15
Q

What are the sodium glucose cotransporter 2 inhibitors?

A

Jardiance

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16
Q

What are drugs with hyerglycemic effects?

A
  • epinephrine
  • glucocorticoids
  • diuretics
  • b2 agonists
  • morphine
  • clonidine
  • phenytoin
  • Ca2+ channel blockers
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17
Q

What are drugs with hypoglycemic effects?

A
  • B2 antagonists
  • Salicylates
  • Ethanol
  • Clofibrate
  • ACE inhibitors
  • Theophylline
  • Sulfonamides
  • Pyridoxine
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18
Q

the primary action of ethanol is to inhibit (blank)

A

gluconeogenesis

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19
Q

In diabetic patients, (blank) pose a risk of hypoglycemia due to their inhibition of catecholamines gluconeogensis and glycogenolysis effects

A

beta blockers

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20
Q

(blank) may mask the sympathetically mediated symptoms associated with the fall in blood glucose (e.g., tremor and palpitations, perspiration).

A

B-blockers

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21
Q

(blank) exert their hypoglycemic effect by enhancing pancreatic -cell sensitivity to glucose to promote insulin secretion in patients able to secrete insulin (some Type 2 diabetics and non-diabetics).

A

Salicylates

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22
Q

Where does SGLT2 inhibitors work and how?

A

inhibits reabsorption of glucose by the kidneys

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23
Q

What does insulin secretatogues do and where do they work?

A

promotes insulin secretion from the pancreas

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24
Q

What does intestinal lipase inhibitor and AGI do?

A

inhibits intestinal lipase (blocks FFA absorption) and glucose absorption in the intestines

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25
Q

What does TZD do and where does it work?

A

Adipose tissues and blocks FFA release

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26
Q

What does Biguanide do and where does it work?

A

blocks glucose release from liver

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27
Q 
What are insulin analgoues? 
How is each type different?
How do you administer them?
What is the half life?
How are they eliminated?
A

insulin preparations

onset and duration of action

subcutaneous injection

9-10 minutes

liver and kidnet

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28
Q

BOLUS (PRANDIAL) INSULINS
What are the rapid-acting (AKA ultra short acting) insulin analogues (clear)?

When is their onset?
When is their peak effect?
What is their duration of action?

What are these types of insulin analogues less associated with which makes them a really good drug?

A

Insulin lispro (takes longer to reach peak and has longer duration of action)
Insulin aspart
Insulin glulisine

Mneumonic: These dont LAG

Onset: 10-15 minutes
Peak: 1-1.5 hrs
Duration: 3-5

less associated with hypoglycemia

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29
Q

BOLUS (PRANDIAL) INSULINS
What are the short acting insulin analogues (clear)?

When is their onset?
peak?
Duration?

A 
Insulin regular (humulin-R)
Insulin regular (novolin)

30 minutes
2-3 hr
6.5 hr duration

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30
Q 
BASAL INSULINS
What are the intermediate-acting insulin analogues (cloudy)?
When is their onset?
peak?
Duration?
A 
Insulin NPH (Humulin)
Insulin NPH (Novolin)
1-3 hr
5-8 hr
up to 18 hr
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31
Q 
BASAL INSULINS
What are the long-acting insulin analogues (clear)?
When is their onset?
peak?
Duration?
A

-Insuin determir (levemir)
-Insulin glargine (lantus)
90 min
not applicable
up to 24 hr (glargine 24hr, determire 16-24 hr)

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32
Q

What type of insulin analogue is this:
(blank) insulin is given 15 minutes prior to a meal and has its peak effect 30-909 minutes after injection (vs 50-120 minutes for regular insulin)

A

Lispro

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33
Q

What type of insulin analogue is this:

(blank) can be given anywhere from 15 minutes prior to 20 minutes after beginning a meal.

A

Lispro

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34
Q

What type of insulin analogues are these:
Soluble, crystalline zinc insulin, usually give S.C, rapidly lowers gluce levels. Made with genetically engineered bacteria

A

Short-acting insulins (clear)

-Insulin regular (humulin, novoline)

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35
Q

What is this:
a suspension of crystalline zinc insulin combined with protamine (a polypeptide). The conjugation with protamine delays its onset of action and prolongs it effectiveness. It is usually given in combination with regular insulin.

A

Intermediate-acting insulins (cloudy)

  • Insulin NPH (humulin)
  • Insulin NPH (Novolin)
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36
Q

What is this:

Precipitation at the injection site extends the duration of action of this preparation.

A

Long-acting basal insulin analogues (clear)

-Insulin glargine (lantus)

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37
Q

What is this:

has a FA complexed with insulin resulting in slow dissolution.

A

Insulin detemir (levemir)

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38
Q

What are the adverse effects of insulin?

A
  • HYPOGLYCEMIA (happens a lot with ethanol consumption)
  • HYPOKALEMIA
  • weight gain
  • injection complications
  • insulin resistance
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39
Q

What are the symptoms of hypoglycemia induced by insulin?

A 
short effect agents: sweating, hunger, palpitations, tremor, anxiety, increased HR, diaphoresis, MS changes,
Long effect agents:
Neuroglycopenic symptoms (such as difficulty in concentratins, confusion, weakness, drowsiness, unconsciousness)
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40
Q

Why do you get hypokalemia with insulin use?

A

insulin draws K+ into the cell with glucose

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41
Q

What are the injection complications that can occur with insulin use?

A
  • IgE mediated local cutaneous reactions

- Lipodystrophy at injection site

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42
Q

What can cause acute insulin resistance?

Chronic?

A 
acute-stress
chronic- 
1) AIRA (antiinsulin receptor autoantibody)
2) down regulation of receptor
3) dysfunction of glucose transfer
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43
Q

Healthy, non-diabetic individuals usually maintain a blood glucose profile of 60 – 100 mg/dl overnight and before meals, and <(blank) mg/dl (ADA goals).

A

90-130

180

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44
Q

What is a bonus dose and how does it work?

A

give 1 unit of rapid acting insulin for 12-15 g of carbs
or
for high blood sugar correction, 1 unit of rapid acting insulin to drop 50 mg/dl blood sugar (depends on individual sensitivity)

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45
Q

From quickest effects to slowest and longest effects put all the types of insulin in order.

A 
Rapid (lispro, aspart, glulisine)
Short (regular)
Intermediate (NPH)
Long (Determir)
Long (glargine)
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46
Q

What is the general calculation for total daily insulin?

A

TDI=body weight (lbs) / 4

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47
Q

What is the basal/background insulin dose equation?

A

50% X TDI

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48
Q

What is the carbohydrate coverage ration (CHO)?

A

500 / TDI dose= 1 unit insulin cover grams of 12g/ CHO

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49
Q

What is the high blood sugar (HBS) correct factor equation?

A

1800 / TDI= 1 unit insulin drops 45 mg/dl blood sugar

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50
Q

(blank) are effective and convenient for the treatment of type 2 DM who do not respond adequatley to non-medical interventions (diet, exercise and weight loss).

A

Oral hypoglycemics

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51
Q

Newly diagnosed type 2 diabetes often respond well to (blank)

A

oral agents

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52
Q

Patients with long standing disease require (blank)

A

combo of agents with or without insulin

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53
Q

The progressive decline (blank) function often necessitates the addition of insulin at some time in the tx of type 2 diabetes

A

b-cell function

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54
Q

What is the first widely used oral anti-hyperglycemic medication?

A

sulfonylureas

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55
Q

What are the first gen sulfonylureas?

A

tolbutamide, chlorpropamide

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56
Q

What are the second gen sulfonylureas?

A

glyburide (glibenclamide), glipizide, glimepiride

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57
Q

What do sulfonylureas do?

A

promote secretion of insulin from B-cells (secretagogues)

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58
Q

What is the mechanism behind sulfonylureas?

A
  • block ATP sensitive K+ channels (Katp) ->depolarization->opening of Ca2+ channel influx->promotes insulin secretion
  • increased number of insulin receptors
  • reduce glucagon secretion and increase binding of insulin to target tissues.
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59
Q

What do sulfonylureas require?

A

normal B cells

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60
Q

What do sulfonylureas bind to?
How are they metabolized?
How are they excreted?

A

Bind to plasma proteins
Metabolized in liver
Excreted by liver or kidney

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61
Q

What are the short acting sulfonylureas? What is the onset and duration?

A

Tolbutamide (Orinase)

6-12 hrs

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62
Q

What are the intermediate acting sulfonylureas?

A

Tolazamide (tolinase)
Glipizide (glucotrol)
Glyburide (Diabeta)

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63
Q

What are the long action sulfonylureas?

A

Chlorpropamide, Glimepiride (24 hours)

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64
Q

What do you use sulfonylureas for?

A

-Type 2 DM
only
Best with patients >40 year-old, Type 2 DM <10 years
(NOT INDICATED IN TYPE 1 patient because it requires normal B cells to work)

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65
Q

Typical reductions in A1C value for second generation of sulfonylureas is (blank)%

66
Q

You can you use sulfonylureas in combination with what 2 drugs?

A

metformin and glitazones

67
Q

What are the adverse effects of sulfonylureas?

A
  • Weight gain
  • Hyperinsulinemia
  • Hypoglycemia (hepatic or renal insufficiency causes accumulation of these agents promoting risk of hypoglycemia)
  • a number of drug-drug interaxns
68
Q

(blank) patients aer particularly susceptible to toxicities of sulfonylureas

69
Q

(blank) is associated with a 2.5X increase in cardiovascular mortality due to arrhythmias and sudden death

A

tolbutamide

70
Q

What four drugs displace sulfonylureas from plasma proteins causing increased hypoglycemic action of sulfonylurea drugs.

A

Clofibrate
Phenylbutazone
Salicylates
Sulfonamides

71
Q

What 5 drugs decrease urinary excretion of sulfonylureas or their metabolites causing increased hypoglyceic action of sulfonylurea drugs?

A 
Allopurinol
Probenecid
Phenylbutazone
Salicylates
Sulfonamides
72
Q

What four drugs reduce hepatic metabolism of sulfonylureas and increase hypoglycemic action of sulfonylurea drugs?

A

Dicumarol
Chloramphenicol
MAOIs
Phenylbutazone

73
Q

What are the non-sulfonylureas?

A

meglitinides:
- Repaglinide
- Nateglinide

74
Q

What do meglitinides (repaglinide, nateglinide) do? Are they long acting or short acting?

A

Promotes the production and secretion of insulin from B-cells (secretagogues) by blocking the same Katp channels as sulfonylureas and cause secretion of insulin.
-short acting

75
Q

When do you take non-sulfonylureas (meglitinides)?

A

taken with or shortly before meals to boost insulin reponse to each meal. (if a meal is skipped, the medication is also skipped)

76
Q

What is the reduction of AIC with non sulfonylureas (meglitinidies)?

77
Q

Meglitinides (repaglinide, nateginide) that reach effective plasma levels when taken (blank) minutes before meals. These agents are metabolized to inactive products by (blank) and is excreted in the (blank)

A

10-30 minutes
CYP3A4
Bile

78
Q

What are the adverse reactions of meglitinides (repaglinide, nateglinide)?

A

-weight gain and hypoglycemia (less than sulfonylureas)
-drug interaxns
(CYP3A4 inhibitors prolong their duration and CYP3A4 promoters decrease their effectiveness)

79
Q

The combination of (blank) and repaglinide has been reported to cause severe hypoglycemia

A

gemfibrozil

80
Q

What are the CYP3A4 inhibitors?

A

Ketoconazole
Fluconazole
Erythromycin

81
Q

What are the CYP3A4 promoters?

A

Barbiturates, carbamazepine

Rifampin

82
Q

What class of drug are biguanides and what drugs are in this?

A

Insulin sensitizers

-Metformin, Phenformin, Buformin

83
Q

(blank) is the principal biguanide used in clinics

84
Q

How do biguanides (metformin) work?

A

reduces hepatic glucose output and increases glucose uptake and utilization by the periphery target tissues.

85
Q

What does metformin require to work?

A

insulin (but does not promote insulin secretion)

86
Q

(blank) is the only oral hypoglycemic shown to reduce CV mortality

87
Q

Can you use metformin with other oral agents and insulin?

A

yes totally!

88
Q

What is the mechanism of action of biguanides

A

reduces plasma glucose levels by….

  • decreasing hepatic glucose production by inhibiting hepatic gluconeogenesis
  • decrease intestinal absorption of sugars
  • increase peripheral glucose uptake
  • increase insulin sensitivity
  • decreased hyperlipidemia
  • decreased appetite
89
Q

What are the clinical uses of metformin?

A

FIRST-line meds for type 2 DM

90
Q

How do you give metformin?

A

give wth diet and exercise

-give extended release form for people with GI problems

91
Q

What are the adverse effects of metformin?

A
  • GI SEs
  • lactic acidosis (mainly with phenformin and buformin)
  • Drug interaxns (cimetidine, furosemide, nifedipine, cationic drugs such as digoxin, amiloride, quinidine ranitidine, and others)
92
Q

What is metformin contraindicated in?

A

1) renal insufficiency
2) hepatic insufficiency
3) congestive heart failure and conditions with hypoxemia, dehydration, or sepsis;
4) metabolic acidosis.

93
Q

If given metformin, (blank and blank) function should be monitored frequently.

A

renal and hepatic

94
Q

If you have a serum creatinine level greater than (blank) in females, or (blank) in males then you should not give metformin due to renal dysfunction

95
Q 
What class of drug do thiazolididinediones belong and what drugs are thiazolididinediones?
What do they need to be effective?
A

Insulin Sensitizers

  • Prioglitazone
  • Rosigglitazone

insulin is necessary for them to be effective

96
Q

What is the mechanism of action of thiazolidinediones?

A

activate nuclear perioxisome proliferator-activated receptor (PPARgamma) (regulates transcription of adipocyte prodution)

  • increase insulin sensitivity of adipocytes, hepatocytes and skeletal muscles
  • increase insulin-dependent glucose disposal
  • decreased insulin resistance
97
Q

What do thiazolidinediones do in the liver?
In the muscle?
In adipose?

A

liver- decreased glucose production and output
muscle- increase glucose uptake
adipose- increase glucose uptake and decrease FA release

98
Q

What are the clinical uses of Thiazolidinediones (pioglitazone, rosiglitazone)?

A

-type 2 DM

99
Q

Which thiazolidinediones can be used with insulin? Which can be used with other hypoglycemic but severe edema occurs when combined with insulin?

A

pioglitazone

rosiglitazone

100
Q

What are thiazolidinediones bound to?
How do they get metabolized?
How are they excreted?

A
  • albumin
  • extensive p450 metabolism
  • metabolite excreted in urine and primary compound is excreted in bile
101
Q

What are the adverse effects of thiazolidinediones?

A
  • Fatal hepatotoxicity

- interaxn w/ oral contraceptives (decrease contraceptive level. ie possible pregnancies)

102
Q

Which thiazolidinediones may possibly linked to bladder cancer?

A

pioglitazone

103
Q

Which thiazolidinediones may possibly linked to coronary heart disease and heart attack?

A

rosiglitazone

104
Q

(blank) may cause or exacerbate CHF. After initiation and dose increases, observe patients carefully for signs and symptoms of heart failure. Initiation of these drugs in patients with established NYHA class III or IV heart failure is contraindicated

A

Pioglitazone

105
Q

What are the alpha-glucosidase inhibitors?

A

Acarbose and miglitol

106
Q

What is the mechanism of action of acarbose and miglitol?

A

saccharides that act as competitive inhibitors of enzymes needed to digest competitors. Specifically they inhibit the alpha-glucosidase in the brush border of the small intestines

107
Q

What are the 2 things that acarbose block?

A
  • Inhibits intestinal membrane bound alpha-glucosidases (decreased glucose)
  • inhibits prancreatic alpha- amylase (decreases glucose)

STARCH BLOCKER

108
Q

In diabetics what are the short term effects of acarbose? long term effects?

A

short term- decrease current blood glucose levels

long term- small reduction in A1c level (typically 0.5-1.0%)

109
Q

What are the clinical uses of alpha-glucosidase inhibitors?

A

Type 2 DM (asian countries, high carb eating patient (eastern food)

110
Q

When should acarbose be taken? Is it effective?

A

start of meal

depends on the amount of complex carbs

111
Q

What are the pharmokinetics of acarbose?

A
  • poorly absorbed in intestinal lumen
  • migitol is absorbed and excreted by the kidney
  • works its magic in the intestinal lumen
112
Q

What are the adverse effects of alpha-glucosidase inhibitors?

A
  • GI (flatulence, diarrhea, cramping), dose-dependent, start with low dose, not be used in diabetics with intestinal pathology
  • Hypoglycemia (correctable only by monosaccharides glucose tablets or gel, not by complex carb such as fruit juice and chocolate)
  • hepatitis, liver enzymes should be check before and during use of this medicine
  • metformin bioavailability is severely decreased when used concomitantly
113
Q

What are the contraindications of alpha glucosidase inhibitors (acarbose)?

A

Mainly GI problems

  • hypersensitivity to the drug
  • diabetic ketoacidosis or cirrhosis
  • IBD, colonic ulceration, intestinal obstruction
  • conditions with increased gas formation in the intestine
114
Q

(blank) are naturally occuring hormones that the gut releases throughout the day. the level of these increases significantly when food is ingested.

115
Q

What are the 2 major incretins in humans that facilitate the response of the pancreas and liver to glucose fluctuations through their action on pancreatic B cells and a cells?

A

Glucose-dependent insulinotropic peptide (GIP) and glucagon-like peptide 1 (GLP-1)

116
Q

(blank) and (Blank) are derived from propeptides, secreted by the GI track, and both stimulate glucose-dependent insulin release from pancreas.

A

GIP (K cells in proximal GI) and GLP-1 (L cells in distal GI)

117
Q

(blank) decreases glucagon production from pancreatic alpha cells when glucose levels increase

118
Q

Incretins cause increase insulin production and decreased glucagon secretion reduces (blank) production when plasma glucose is elevated

A

hepatic glucose

119
Q

The physiologic activity of incretins is limited by the enzyme (Blank) which rapidly degrades active incretins after their release

A

dipeptidyl peptidase-4 (DPP-4)

120
Q

The incretin effect is diminished in (blank).

What exactly causes this diminishment?

A

Type 2 diabetes

  • > release of GLP-1 is defective and levels of GLP-1 is decreased.
  • > the insulinotropic response to GIP is diminished but not absent
121
Q

What are the DPP-4 inhibitors?

A

Sitagliptin (Januvia)

Saxagliptin (onglyza)

122
Q

What is the mechanisms of action of DPP-4 Inhibitors?

A

Reduces blood glucose levels by inhibiting DPP-4 and increasing the levels of GLP-1 and GIP

123
Q

What are the clinical uses of DPP-4 inhibitors (Sitagliptin: januvia))?

A

-Type 2 DM (either alone or in combo with oral hypoglycemics (such as metformin or a thiazolidinedione)

124
Q

What are the adverse SEs of DPP-4 inhibitors?

A
  • rare nausea and common cold like symptoms
  • photosensitivity
  • no signif hypoglycemia when use alone (but may happen with combination)
  • heart failure
  • pancreatitis (some fatal) in people treated with sitagliptin and other DDP-4 inhibitors
  • renal failure and hypersensitivity reactions (but a causative role for sitagliptin has not been established)
125
Q

What is the glucagon like peptide 1 (GLP-1) analogue?

A

exenatide (byetta)

126
Q

What is the mechanism of action of exenatide (byetta)?

A
  • augment pancreas response (increases insulin released to appropriate levels)
  • suppresses pancreatic release of glucagon in response to eating
  • slows gastric emptying (slows time glucose is in bloodstream)
  • reduces appetite, promotes satiety via hypothalamic (slowsly causes weight loss)
  • reduces liver fat content
127
Q

What are the clinical uses of GLP-1?

A
  • Substitute mealtime insulin
  • adjunct to improve glycemic control in pnts taking (metformin, sulfonyurea or thiazolidineiones) meds with type 2 DM
  • monotherapy for type 2 DM
  • NOT FOR type 1 -> ehances release of endogenous insulin from pancreas
128
Q

How do you take GLP-1?

A

injected SC twice a day, before the morning and evening meal. Must be used within 60 minutes (1 hr) before eating the meal and should be given at least 6 hours apart. Do not use after eating a meal.

129
Q

T or F
you can use Exenatide for treating diabetic ketoacidosis in patients with type 1 diabetes or as a substitute for insulin in patients who require insulin

130
Q

What are the adverse SEs of Exenatide?

A
  • GI disorders
  • acid or sour stomach
  • heartburn, belching, diarrhea, indigestion, n/v
  • hypoglycemia
  • dizziness, headache, feeling jittery
  • possible increase in thyroid cancer
131
Q

What are the drug interactions associated with exantide?

A

delayed or reduced concentrations of lovastatin, paracetamol (acetaminophen) and digoxin

132
Q

(blank) is a sodium glucose co-transporter 2 (SGLT2) inhibitor. How does it work?

A

Jardiance
-blocks reabsorption of glucose (blood sugar) by the kidneys, increase glucose excretion in urine and lowering blood sugar levels in people with diabetes. i.e. makes you pee out glucose

133
Q

What are the clinical uses of SGLT2 inhibitors (Jardiance)?

A

-adjunct to diet and exercise to improve glycemic control in adults with type 2 DM

134
Q

Patients should not take jardiance if they have (blank) or are on (Blank) or if they are allergic to (blank) or any ingredient in jardiance.

A

kidney problems
dialysis
empagliflozin

135
Q

Do you use jardiance in type I or type 2 diabetics?

A

type 2 diabetics

dont use in type 1 or ketoacidosis

136
Q

What are the adverse SEs of Jardiance (SGLT2 inhibitors)?

A

dehydration
low BP
dizziness or fainting

137
Q

In the treatment and control of diabetes, you should try to get to target within (blank) months of diagnosis

138
Q

If you have a initial A1c of less than 8.5% how do you treat your patient?

A

start metformin OR reassess in 2-3 months then decide on starting metformin

139
Q

If you have an initial A1C of equal to or greater than 8.5%?

A

start metformin or consider combo therapy to achieve greater than 1.5% A1C reduction

140
Q

If you have symptomatic hyperglycemia and metabolic decompensation what are the symptoms? What should you be considered with? what should you give?

A 
polyuria
polydipsia
weight loss
volume depletion
-insulin deficiency
-insulin +/- metformin
141
Q

At the diagnosis of type 2 diabetes, start lifestyle intervention, if A1C is less than 8.5% and your patient isnt at glycemic target by 3 months start (blank).

A

start or increase metformin

142
Q

At the diagnosis of type 2 diabetes, start lifestyle intervention, if A1C is greater than 8.5% start (blank).

A

start metformin immediately

-consider initial combo with another antihyperglycemic agent

143
Q

At the diagnosis of type 2 diabetes, start lifestyle intervention, if your patient has symptomatic hyperglycemia with metabolic decompensation start (blank).

A

initiate insulin +/- metformin

144
Q 
What drug is this:
decreases Relative A1C 
rarely causes hypoglycemia
-reduces weight
-improved postprandial control, GI SE
A

Acarbose (alpha-glucosidase inhibitor)

145
Q 
What drug is this:
reduces A1C very well
Rarely causes hypoglycemia
decreases weight really well
has GI SEs
Very expensive!
A

incretin agents: DPP-4 inhibitors and GLP-1 receptor agonists

146
Q 
What drug is this:
lowers A1C really well
causes hypoglycemia
increases weight
no dose ceiling, flexible regiments
147
Q

What drug is this:

  • decreased A1C
  • causes hypoglycemia
  • increases weight
  • Less hypoglycemia in context of missed meals but usually required TID or QID dosing
A

Insulin secretagogues: meglitinide (expensive)

sulfonylureas

148
Q

Gliclazide and glimepiride associated with less hypoglycemia than (blank)

149
Q 
What drug is this:
decreases A1C
hypoglycemia (rare)
increased weight
CHF, edema, fractures, rare bladder cancer (pioglitazone), CV controversy (rosiglitazone), 6-12 weeks required for max effect
150
Q 
What drug is this
lowers A1C
doesnt cause hypoglycemia
decreases weight 
Gi side effect
very expensive
151
Q

What is the only drug that is safe for patients with renal failure?

A

Repaglinide

thiazolidenediones and linaglipitin are okayish

152
Q

What is the worst drug to be used for a patient wtih renal failure?

A

Luraglutide

153
Q

In people with type 2 diabetes, if glycemic targets are not achieved using lifestyle management within (blank) months, antihyperglycemic agent therapy should be initiated

154
Q

If A1C ≥8.5%, antihyperglycemic agents should be initiated concomitantly with lifestyle management, and consideration should be given to initiating combination therapy with 2 agents, one of which may be (blank)

155
Q

Individuals with symptomatic hyperglycemia and metabolic decompensation should receive an initial antihyperglycemic regimen containing (blank)

156
Q

What is the initial drug used for overweight patients with diabetes

157
Q

Intensive therapy results in (blank) fold increase in frequency of hypoglycemia

158
Q

Many clinicians believe the increased risk of hypoglycemia that accompanies intensive therpay is justified by the substantial decrease in the incidence of long-term complications such as (blank and blank) .

A

diabetic retinopathy and nephropathy

159
Q

How does intensive insulin therapy effect patients with type I diabetes?

A

Reduces:
retinopathy
nephropathy
neuropathy

160
Q

How does intensive insulin therapy effect patients with type 2 diabetes?

A

reduces:
retinopathy
nephropathy

161
Q

What does xiao-ke-wan do?

A
  1. Absorption
  2. Expansive action
  3. Increase intestine peristalsis
  4. Nourishing action

Block 10 Week 2 (7 decks)

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