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pharm exam 3 > drug therapy for diabetes mellitus > Flashcards

drug therapy for diabetes mellitus Flashcards

1
Q

what is glucose

A

sugar in the blood, body primary energy source, brain almost exclusively. uses glucose for energy

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2
Q

what two major hormones stabilize glucose levels

A

glucagon and insulin

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3
Q

alpha cells secrete

A

glucagon, increase blood glucose levels

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4
Q

glucagon stimulates

A

the liver to convert some stored glycogen to glucose to use by the body

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5
Q

beta cells secrete

A

insulin, decrease blood glucose levels

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6
Q

glucagon is secreted with

A

low blood glucose; helps to maintain glucose between meals, works with insulin to maintain levels

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7
Q

glucose levels; between meals

A

decreased blood glucose -> into pancreas -> decreased insulin & increased glucagon secretion -> into liver -> release of stored glucose, breakdown of fat

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8
Q

glucose levels; after a meal

A

increased blood glucose -> into pancreas -> increased insulin secretion & decreased glucagon secretion -> into liver -> cellular uptake of glucose

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9
Q

insulin after a meal

A

pancreas recognizes rising glucose, secretes insulin to lower blood glucose; without insulin, glucose unable to enter cells

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10
Q

how does insulin act as transport to allow cells access to glucose

A

glucose can enter cells, cells store glucose as glycogen, converts lipids to fat, increase protein synthesis and stop glycogenesis

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11
Q

insulin helps to ______ glucose (blood sugar) when

A

lower blood sugar when levels are too high

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12
Q

hormones that can increase glucose

A

epinephrine, thyroid hormone(metabolism), growth hormone, glucocorticoids(steroids, promote glucose production in liver)

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13
Q

drugs that can increase glucose

A

phenytoin, beta blockers, NSAIDs, diuretics

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14
Q

drugs that can decrease glucose

A

alcohol, lithium, ACE inhibitors

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15
Q

what is diabetes mellitus

A

chronic metabolic disorder in which there is deficient insulin secretion or decrease sensitivity of insulin receptors resulting in hyperglycemia

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16
Q

classifications of DM

A

type I and type II

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17
Q

what is type I diabetes mellitus

A

common chronic disorder of childhood/ autoimmune disorder that destroys pancreatic beta cells difficult to control, sudden onset between ages 4-20, high incidence of complications and difficult to control, requires exogenous insulin administration

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18
Q

type I diabetes is dependent diabetes meaning

A

you have to administer insulin

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19
Q

what is type II DM

A

characterized by hyperglycemia and insulin resistance/ (beta cells are present and insulin present but unable to work), onset after age 40 years/ increasing prevalence among children and teens, gradual onset with less severe symptoms, 90% of people with diabetes have type 2

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20
Q

risk factors for development of type II DM

A

obesity, sedentary lifestyle, presence of metabolic syndrome, ethnicities (African American & hispanics)

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21
Q

metabolic syndrome r/t diabetes

A

abdominal obesity low HDL, hypertriglyceridemia, hypertension and/or impaired fasting glucose

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22
Q

s/sx of hyperglycemia (diabetes): fasting blood glucose levels greater than 126 mg/dL

A

polyuria, polyphagia (extremely hungry), polydipsia(extremely thirsty), glycosuria (kidneys clearing extra glucose), weight loss (bc of metabolic changes), fatigue

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23
Q

chronic complications of untreated DM

A

macrovascular and microvascular

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24
Q

what is macrovascular (big vessels)

A

HTN, MI, stroke, peripheral vascular disease (PVD)

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25
Q

what is microvascular (little vessels)

A

nephropathy (damage to kidneys), retinopathy (in eyes/ go blind), neuropathy (damage to nerve in PNS -> complete loss of sensation in extremities)

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26
Q

diabetes high risk to extremities

A

Peripheral vascular disease results from narrowing of blood vessels increasing the risk for reduced or lack of blood flow in legs. Feet wounds are likely to heal slowly contributing to gangrene(death of body tissue due to lack of blood flow) and other complications

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27
Q

acute complications of diabetes

A

diabetic ketoacidosis (DKA), hyperosmolar hyperglycemic nonketotic coma (HHNC)

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28
Q

what is diabetic ketoacidosis

A

life threatening, severe insulin deficiency, usually type I/ fat broken down for energy, results in ketones -> ketones reproduce faster than needed which cause a drop in pH (acidosis), usually type 1

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29
Q

symptoms of diabetic ketoacidosis

A

fruity odor to breath, ketones, kussmauls respirations(deep breathing), severe hyperglycemia (> 240), polyuria, polydipsia, N/V, coma

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30
Q

how to treat diabetic ketoacidosis

A

give a lot of IV fluids (flush out extra glucose and flush out some of the acid that’s making our blood so acidic), & give insulin (body can use those cells and reverse DKA)

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31
Q

what is hyperosmolar hyperglycemic nonketotic coma (HHNC)

A

life threatening, severe hyperglycemia, usually type 2; excessive glucose and electrolytes, severe dehydration

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32
Q

symptoms of hyperosmolar hyperglycemic nonketotic coma

A

extremely high glucose >600, polyuria, dehydration, drowsiness, confusion, coma

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33
Q

treatment for hyperosmolar hyperglycemic nonketotic coma

A

give lots of fluid, give insulin to bring down blood sugar

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34
Q

when to check blood sugar

A

before meals and at bedtime, if eating

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35
Q

abnormal fasting glucose number

A

> 126

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36
Q

diabetic AC (before meal, in morning) blood sugar goal

A

70-130

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37
Q

when to check blood sugar if NPO, or tube feeding or TPN

A

check every 6 hours

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38
Q

what is hemoglobin A1C

A

measure average blood glucose over a 3 month period, normal is < 7%

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39
Q

T or F. diabetes mellitus is a chronic, systemic disease characterized only by metabolic abnormalities

A

False; diabetes mellitus is a chronic, systemic disease characterized by a metabolic AND VASCULAR abnormalities. While a major clinical manifestation of DM is hyperglycemia, vacuum problems include atherosclerosis throughout the body, which results in HTN, MI, stroke and PVD

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40
Q

T or F. insulin is a hormone secreted by beta cells in the pancreas

A

true. insulin is a hormone secreted by beta cells in the pancreas that allows rapid entry of glucose into cells

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41
Q

signs of hyper-glycemia

A

Three P’s (polyuria, polyphagia, polydipsia), fatigue, weakness, dry skin (hot & dry= sugar high)

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42
Q

signs of hypo-gylcemia

A

sweating, tremors, tachycardia, hunger, confusion, drowsiness, seizures (cold & clammy= need some candy)

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43
Q

drug therapy for diabetes

A

control glucose levels and prevent complications

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44
Q

treatments for type 1 DM

A

insulin

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45
Q

treatment for type 2 DM; work in different parts of the body

A

sulfonylures, alpha glucosidase inhibitors, biguanide, thiazolidines, meglitinides, DDP 4 inhibitors, amylin analogs, incretin mimetics, SGLT2 inhibitors

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46
Q

what is insulin

A

human product; synthetic product is identical to endogenous insulin, synthesized in laboratories by altering the type or sequence of amnio acids

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47
Q

administration of insulin

A

CANNOT be given orally; most give subQ, regular can be IV; U-100 concentration in U.S. (100units/mL), orange tipped syringe or pen

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48
Q

rapid acting

A

lisper, aspart; rapid onset, shorter duration of action than regular (Onset: 15-30 min, P: 30min-2.5hr, D: 3-6hr)

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49
Q

short acting

A

regular; short onset, short duration of action (onset: 30-60 min, P: 1-5 hr, D: 6-10hr)

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50
Q

intermediate acting

A

NPH; slower absorption, prolonged action (onset: 1-2hr, P: 4-12hr, D: 16hr)

51
Q

long acting

A

glargine, detemir; provide basal insulin over 24 hr period (Onset: 3-4 hr, P: continuous, D: 24hr)

52
Q

ultra long acting

A

degludec; provide basal insulin over 42 hr period

53
Q

mechanism of action for insulin

A

increased glucose uptake by cells, decreased glucose production by liver

54
Q

uses of insulin

A

lower blood glucose, Renault may be given IM or IV in an emergency, can be used in children and older adults

55
Q

contraindication of insulin

A

if they are hypoglycemia

56
Q

timing insulin with meal

A

lispro (rapid): 15-30 mins before a meal, regular (short): 30-60 mins before a meal

57
Q

adverse effects of insulin

A

hypoglycemia, local reactions, so you want to rotate sites

58
Q

drug-drug interactions with insulin

A

any drug that affect glucose levels; beta blockers, MAOIs, NSAIDs, salicylates, alcohol, herbal preparations

59
Q

nursing implications for insulin

A

be aware of mealtimes, rotate injection site (the abdomen is the best), monitor for hypoglycemia during sleep, insulin pumps (regular or rapid acting), considered a high risk medication (know policy)

60
Q

programmed insulin order

A

given to regulate level between meals, set amount ordered, watch nutrition status, make sure patient is eating; if NPO do not give programmed insulin

61
Q

example of programmed insulin order

A

5 units lispro subQ TID AC (with meals). Hold of BS <70

62
Q

sliding scale insulin order (SSI)

A

dosing based on blood sugar level, notify MD if NPO

63
Q

patient teaching about insulin

A

diet, weight control, exercise; know s/sx; teach family what to do; test BS as ordered; what to do if you’re sick; proper subQ injection technique; follow up appts

64
Q

insulin SICK mimetic

A

S:sugar, I:insulin, C:carbs, K:ketones

65
Q

T or F. insulin plays a major role primarily in the metabolism of carbohydrates

A

false; insulin plays a major role in metabolism of CARBOHYDRATE, FAT, and PROTEIN where the nutrients are broken down into simpler molecules (glucose, lipids, and amino acids)

66
Q

for type 2: sulfonylureas; example med

A

glyburide

67
Q

what does sulfonylureas do

A

stimulate pancreas to release insulin; bind to K+ channels on pancreatic beta cells, increase number of insulin receptors

68
Q

what is sulfonylureas used for

A

injections for elevated serum glucose, must have some functioning pancreatic beta cell

69
Q

adverse effects of sulfonylureas

A

hypoglycemia

70
Q

contraindications for sulfonylureas

A

sulfa allergy, renal failure, liver failure

71
Q

drug-drug interactions for sulfonylureas

A

beta blocker, alcohol

72
Q

type 2: alpha glucosidase inhibitors example med

A

acarbose

73
Q

what are alpha glucosidase inhibitors

A

delays digestion of complex carbohydrates; decrease the increase in blood sugar after meals, given in combo with sulfonylurea

74
Q

uses for indications for alpha glucosidase inhibitors

A

decrease in postprandial glucose

75
Q

adverse effects of alpha glucosidase inhibitors

A

hypoglycemia, GI upset

76
Q

contraindications for alpha glucosidase inhibitors

A

hepatic disease, IBS

77
Q

drug-drug interactions for alpha glucosidase inhibitors

A

can decrease digoxin levels

78
Q

nursing implications for alpha glucosidase inhibitors

A

take at beginning of meal

79
Q

type 2 biguanodes example med

A

metformin

80
Q

what are biguanodes

A

decrease hepatic glucose production, increases use of glucose by muscle and fat cells, decreased intestinal absorption of glucose

81
Q

uses for biguanodes

A

insulin resistance; commonly first choice for type 2 DM, used to treat PCOS

82
Q

adverse effects for biguanodes

A

lactic acidosis, GI upset

83
Q

contraindications for biguanodes

A

BLACK BOX warning to avoid over 80 year old, renal failure, ***hold metformin 48hrs before and after contrast media (CT dye, heart cath), testing to avoid renal failure

84
Q

nursing implications for biguanodes

A

take with meals, increased effects if taken with furosemide, digoxin, vancomycin; monitor renal function

85
Q

type 2 thiazolidinediones (TZDs) example med

A

rosiglitaxone

86
Q

what are thiazolidinediones (TZDs)

A

stimulates insulin receptors on muscle, fat, and liver cells

87
Q

uses for thiazolidinediones (TZDs)

A

insulin resistance; used in combo with insulin, sulfonylureas or biguanides

88
Q

adverse effects of thiazolidinediones (TZDs)

A

hepatotoxicity, CHF, weight gain

89
Q

contradictions of thiazolidinediones (TZDs)

A

liver disease, CV disease ***BLACK BOX warning of risk for CHF and MI

90
Q

nursing implications for thiazolidinediones (TZDs)

A

take with meals, monitor liver functions, monitor pts for signs of HF, gemfibrozil may increase effects, may take 12 weeks to reach peak effects

91
Q

type 2 meglitinides example med

A

repaglinide

92
Q

what are meglitinides

A

stimulates pancreatic stimulation of insulin (need working beta cells)

93
Q

uses for meglitinides

A

elevated serum glucose, used in combo with TZDs or biguanide

94
Q

adverse effects of meglitinides

A

hypoglycemia less so than sulfonylureas, GI upset

95
Q

contraindications for meglitinides

A

renal disease, liver disease, type 1 DM

96
Q

nursing implications for meglitinides

A

take before meals (if meal skipped, skip dose; if meal added, add dose), gemfibrozil and itraconazole increase effects

97
Q

type 2 dipeptidyl peptidase 4 inhibitors (DPP-4) example med

A

sitagliptin

98
Q

what are dipeptidyl peptidase 4 inhibitors (DPP-4)

A

balance the release of insulin and limit the release of additional glucose from the liver, inhibition of glucagon secretion, delayed gastric emptying, and induction of satiety (need working beta cells)

99
Q

uses for dipeptidyl peptidase 4 inhibitors (DPP-4)

A

elevated serum glucose, used in combo with TZDs or biguanide

100
Q

adverse effects of dipeptidyl peptidase 4 inhibitors (DPP-4)

A

upper resp tract infections, heart failure

101
Q

contraindications for dipeptidyl peptidase 4 inhibitors (DPP-4)

A

type 1 Dm, insulin use, renal failure

102
Q

nursing implications for dipeptidyl peptidase 4 inhibitors (DPP-4)

A

one daily with or with out meal

103
Q

type 2 amylin analogs example med

A

pramlintide

104
Q

what are amylin analogs

A

suppresses postprandial glucagon secretion, increases sense of satiety

105
Q

uses for amylin analogs

A

regulate the postprandial rise in blood glucose, used in addition to insulin, sulfonylureas or biguanides

106
Q

adverse effects of amylin analogs

A

hypoglycemia ***BLACK BOX warning for severe hypoglycemia if mixed with insulin

107
Q

nursing implications for amylin analogs

A

monitor blood sugars closely, avoid giving with anticholinergics, may promote weight loss, subQ injection before meals

108
Q

type 2 incretin mimetics example med

A

exenatide

109
Q

what are incretin mimetics

A

stimulates the pancreas to secrete the right amount of insulin based on the food that was just given

110
Q

uses for incretin mimetics

A

postprandial glucose elevations, used in combo with oral medications

111
Q

adverse effects of incretin mimetics

A

hypoglycemia, GI distress and nausea, pancreatitis

112
Q

contraindications for incretin mimetics

A

liver disease, ***BLACK BOX warning for risk of thyroid cancer

113
Q

nursing implications for incretin mimetics

A

subQ injection within 1 hour of breakfast and diner, must be refrigerated, some ER versions available (dulaglutide) only need 1/weekly injection, may promote weight loss

114
Q

type 2 sodium glucose contransporter 2 inhibitors (SGLT2) example med

A

canaglifozin

115
Q

what are sodium glucose contransporter 2 inhibitors (SGLT2)

A

blocks reabsorption of glucose In the kidney, promotes excretion of glucose in urine

116
Q

uses of sodium glucose contransporter 2 inhibitors (SGLT2)

A

improved glucose control, used in combo with other anti-diabetics

117
Q

adverse effects of sodium glucose contransporter 2 inhibitors (SGLT2)

A

dehydration, hypotension, electrolyte imbalance, bone loss, increased risk of leg/foot amputations

118
Q

contraindications for sodium glucose contransporter 2 inhibitors (SGLT2)

A

renal failure

119
Q

nursing implications for sodium glucose contransporter 2 inhibitors (SGLT2)

A

take with first meal of day, use caution in combo with meds that decrease BP, risk for dehydration or syncope

120
Q

general patient education about diabetes

A

consistent diet and exercise = best control; maintain normal weight; unopened bottles of insulin stored in fridge; know s/sx and what to do; teach family; maintain BS to prevent complications; follow up appts; don’t start new meds/herbs with put telling MD; alert MD if BS is >250

121
Q

patient education on hyperglycemia management: seek MD if

A

BS > 250, ketones in urine, fever above 101, vomiting & diarrhea, miss multi doses of a med

122
Q

patient education on hypoglycemia management

A

rapidly absorbed sugar (10-20mins), if patient is alert (4oz of juice/soda, 1 tube glucose gel, 2-3 glucose tabs), if patient is unable to swallow (dextrose 50% half ampule, glucagon IM/SQ), avoid taking so much sugar that you cause hyperglycemia

123
Q

managing diabetes on sick days

A

illness can cause stress response and increase bS, continue to take anti-diabetic meds, test for ketones in urine, check glucose at least 4x daily, if unable to continue liquids (15g carbs every 1-2 hrs, gatorade, drink 2-3 quarts of fluids, water)

124
Q

a patient with type 2 DM is scheduled for a heart catheterization in 1 week. The nurse instructs the patient to stop taking which med 2 days before the procedure

A

metformin; biguanides like metformin can cause kidney failure if given 48 hrs before or after receiving contrast dye

pharm exam 3 (5 decks)

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