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Nursing, LPN, Year 2 > X Diabetes Mellitus - Burke Ch 36 > Flashcards

X Diabetes Mellitus - Burke Ch 36 Flashcards

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1
Q

Definition of Diabetes Mellitus

A

a group of systemic metabolic disorders characterized by hyperglycemia

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2
Q

How much of US population is Diabetic?

A
  1. 1 mil, 9.3% of population
    - 21 mil Dx
    - 8.1 mil Un Dx
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3
Q

Diabetes interferes w ability to use?

A

Glucose

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4
Q

What is Glucose?

A

Simple sugar, monosaccharide

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5
Q

What is glucose used for and by

A

Used by cells for energy

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6
Q

Does brain need insulin?

A

No, brain only uses glucose. When none available, brain cells die

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7
Q

Glucose comes from ?

A

Carbs broken down into sugar.

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8
Q

End products of digestion?

A

Protein, fats, carbs

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9
Q

Carbs break down to….

A

Glucose, fructose, lactose

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10
Q

Fats (lipids) break down to….

A

Fatty acids, glycerol

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11
Q

Protein breaks down to…..

A

Amino acids

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12
Q

Pathway of glucose from intestines…..

A

Intestines absorb water And nutrients……glucose to blood……from blood to cells……

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13
Q

Where is excess glucose stored?

A

Liver and adipose and muscles

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14
Q

Explain lock and key method

A

Insulin attached to insulin receptor, opens door, allows glucose in.

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15
Q

Stimulus for insulin release?

A

Body senses UP glucose and stimulates pancreas to release insulin

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16
Q

Excess glucose converted to ? Stored where?

A

Converted to glycogen and stored in liver

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17
Q

Organs involved in BG regulation?

A

Pancreas and liver

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18
Q

What is glucagon?

A

Pancreas releases glucagon when senses LO BG, glucagon stimulates liver to break down glycogen into glucose.

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19
Q

Glycogen bs Glucagon

A

Glycogen lowers BG

Glucagon raises BG

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20
Q

Some fictions of liver

A
  • Regulate BG
  • Synthesis and storage of amino acids, proteins, vits, fat
  • detox
  • blood circulation and filtration
  • bile drainage
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21
Q

What other sources of energy can the body use other than carbs

A

fat

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22
Q

what are complications of metabolizing fat for energy?

A

ketones are released. Too many ketones in body give off fruity breath. (acetone)

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23
Q

what does buildup of ketones do to body’s pH

A

acidotic

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24
Q

3 Ketone bodies?

A

AHH….

Acetone, Acetoacetic Acid, Hydroxybutyric Acid

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25
Q

normal body pH

A

7.35 - 7.45 pH

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26
Q

Ketosis

A

presence of ketone bodies in blood

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27
Q

Ketonuria

A

ketones eliminated in urine

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28
Q

common people ketones found in?

A

starving, fasting, diabetic

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29
Q

Glycogen

A

storage form of glucose. stored in liver

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30
Q

Glucagon

A

Hormone secreated by pancreas in response to LO BG, stimulating liver to breakdown glycogen into glucose

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31
Q

Insulin

A

Hormone secreted by Pancreas to LOWER BL levels

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32
Q

DM risk factors

A
  • Diet/Lifestyle (diet hi in fried, carbs and sweets)
  • Aging
  • Obesity
  • Genetic pre-disposition
  • virus
  • T-lymph/autoimmune
  • race
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33
Q

Non-Modifiable risk factors for NIDDM

A
  • Family Hx
  • Race/Ethnicity
  • Age
  • Hx of gestational diabetes. chance of devoping later in life.
  • Gave birth to large UP 9lb baby.
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34
Q

Races at risk of NIDDM

A 
Af-Am
Latino
Asian Am
Native Am
Pacific Islanders
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35
Q

Modifiable risk factors for NIDDM

A
  • overweight/obese (50% men, 70% women w diabetes are obese)
  • Physical inactivity
  • Hypertension
  • UP alchohol consumption
  • smoking (18-24 cigs per day)
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36
Q

How much of US population is pre-diabetic

A

86 mil
1/3 adults are pre-diabetic
9/1 adults don’t know they are

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37
Q

Definition of Pre-Diabetics

A

BG levels are abnormal (80 - 100mg/dL) but don’t meet criteria for being diabetic

11% of PD develop DM within 1 year

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38
Q

common Dx tests

A
  • Hb A1C (glycosylated Hemoglobin)
  • FBG, Fasting Blood Glucose
  • OGTT, Oral Glucose Tolerance Test (drink bottle fast, test BG in 1 hr)
  • serum Insulin
  • C-Peptide test
  • Post Prandial Blood Sugar (2 hr after meal)
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39
Q

What does it mean if glucose is in the urine?

A

Body is not absorbing it, causing build up and spill over

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40
Q

Insulin made in what part of Pancreas? by what cells?

A

Islets of Langerhorn by B cells

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41
Q

Types of DM

A
  • Type 1, IDDM (Juvenile)
  • Type II, NIDDM
  • Gestational
  • Other: Meds (long term steroid use, Chemo), Organ Transplant Recipients, Trauma to Pancreas, Cancer of Pancreas)
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42
Q

How common is Type I

A

5-10% of cases

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43
Q

IDDM, Pathos, Cause

A
  • Insulin Dependent Diabetes Mellitus
  • Progressive destruction of B cell function (lose ability to secrete Insulin)
  • Cause unknown
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44
Q

How does blood work show Type I?

A

Islet cell antibodies. Means body is attacking the Islet cells

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45
Q

upon Dx, how many B cells are destroyed?

A

80-90%

within 5 years, 100% will be destroyed

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46
Q

How does Type I lead to Hyperglycemia?

A

No insulin. Body BG UP, body can’t use glucose for energy, blood becomes Hyperglycemic.

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47
Q

How are symptoms displayed in IDDM?

A

Sudden Onset. Usually discover when body goes into DKA. Diabetic Keto Acidosis

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48
Q

DKA

A

Diabetic Keto Acidosis

when body starts metabolizing fat, creating ketones in the body. Ketones make body acidotic.

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49
Q

NIDDM

A
  • Non-Insulin Dependent DM
  • Type II
  • Gradual onset of symptoms. Body always making some insulin, but insufficient amounts
  • Insulin RESISTANT rather than LACK of insulin
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50
Q

Insulin Resistance

A

cells become resistant to effect of Insulin. More insulin needed for same effect.

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51
Q

Causes of Insulin Resistance

A
  • Obesity
  • Metabolic Syndrome
  • Pregnancy
  • Infection
  • Stress
  • Long term steroid use
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52
Q

Rx for Type I vs Type II

A

Insulin vs Diet, exercise, meds

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53
Q

Incidence of complications for Type 1 v Type II

A

both frequent

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54
Q

High BG complications for Type 1 v Type II

A

DKA (metabolize fat) vs Hyperglycemic, hyperosmolar, nonketotic syndrome

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55
Q

Usual age onset Type 1 vs Type II

A

40 and below vs 40 and up

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56
Q

Body weight of Type 1 vs Type II

A

lean vs Obese

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57
Q

Onset of SS for Type I vs Type II

A

sudden vs gradual

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58
Q

When do mothers usually find out about Gestational Diabetes

A
  • ~ 28wks at time of OGTT
  • 2-10% of US pregnancies
  • Rx, Glucose control, diet, excercise
  • Risk of dev DM later in life
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59
Q

Macrosomomia

A

Big Baby, over 9lbs. due to uncontrolled insulin production and UP BG in mom and baby during gestation

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60
Q

Women w Gestational DM have 30-65% chance of

A

developing DM in 10-15yrs

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61
Q

Glycosuria

A

glucose in urine

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62
Q

Gluycosuria –> Polyuria –> Polydipsia

A

Hyperclycemia –> Polyphagia

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63
Q

Difference between Glycogen and Glucagon?

A

Glycogen - stored in liver

Gloucagon - Hormone that breaks down Glycogen to Glucose.

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64
Q

3 Ps?

A

Polyuria - frequent urination
Polydipsia - frequent drinking
Polyphagia - frequent eating

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65
Q

Other S/S of DM

A
  • Nausea
  • Cold extremities
  • blurred vision
  • halos (vision)
  • Neuropathy (nerve pain)
  • LO sensation to pain/temp in feet
  • Impotence (ED)
  • Slow wound healing
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66
Q

Hirsutism

A

in Type I, male pattern hair growth in women (beard)

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67
Q

Dx test for PreDiabetes (only need 1 out of 3 to be diagnosed)

A
  • Fasting BG (100 - 125 mg/dL)
  • Elevated Hba1c (5.7 - 6.4)
  • 2hr Oral Glucose Tolerance (140-199mg/dL)
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68
Q

DM Dx tests (only need 1 out of 4 to be diagnosed)

A
  • Elevated fasting BG on 2 occassions (>126mf/dL)
  • Casual BG level (>200mg/dL w 3 classic Ps)
  • OGTT w 2hr BG (>200mg/dL)
  • Hba1c (>6.5%)
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69
Q

Fasting BG test steps

A

1) Fast for 8 hrs
2) obtain blood sample
3) normal = 99mg/dL or less

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70
Q

Normal BG Ranges for Adults

A

-Preprandial glucose (before meal) =

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71
Q

What does OGTT measure and recomendations

A

this test involves drawing a fasting blood test, followed by having a person drink a 75-gram glucose drink and then drawing another sample two hours after consuming the glucose.

  • ability to use glucose
  • NPO for 8-12hrs before test
  • no smoking, caffeing
  • drink glucose drink
  • test 2 hrs later (pregnant women only wait 1 hr)
  • ptn can drink water during test
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72
Q

Normal Insulin levels

A

5-24mcU/mL

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73
Q

Serum Insulin test steps

used to dx ?

A

1) NPO for 8 hrs
2) obtain blood sample

diagnose IDDM
abnormal: no insulin present. in NIDDM, level will be normal to High

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74
Q

Post Prandial Blood Sugar test steps

A
  • 12hr fasting. BG done before meal
  • eat entire meal (75g of CHO)
  • rest and no smoking after meal
  • Blood sample obtained 2 hrs after meal

if result >200mg/dL = DM
if result 140 - 160 = Pre DM
if result

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75
Q

Glocosylated Hemoglobin (HbA1c) test steps

A
  • monitors Rx, Dx DM, How well controlled DM is
  • 2-3 mos blood sugar average
  • shows Hgb to which glucose is bound
  • no fasting required
  • results

A1c Level
Normal - or equal 6.5%

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76
Q

C-Peptide Test steps

A
  • Determines insulin production. (for every insulin produced, 1 c-peptide made)
  • identify’s pts who secretly seld administer insulin = Facticious Hypoglycemia
  • C-Peptide levels corrolate 1:1
  • NPO 8 hrs prior
  • obtain blood sample
  • Normal fasting level = .78mg/ml

Can distiguish btwn Type I and II. NO insulin produced = no cpeptide produced.

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77
Q

Facticious Hypoglycemia

A

when patients deliberately administer insulin to create hypoglycemia (suicide?)

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78
Q

DISEASE
Fasting Sugar >120
OG TT > or equal 200
HbA1c >6.5

PRE-DISEASE
Fasting Sugar 100-125
OGTT 140-199
HbA1c = 5.7-6.4

NORMAL
Fasting Sugar 99 or less
OGTT

A

.

79
Q

People w Diabetes are at higher risk of developing …..?

A

heart disease & stroke

80
Q

DM is the ? leading cause of ? in the US

A

6, death

81
Q

What virus’ trigger Type 1 DM?

A

Mumps/Rubella, Coxsackie 4

82
Q

Lantus is a type of ?

A

long acting insulin

83
Q

Name of Intermediate acting Insulin?

A

NPH, NovolinkR, HumalinR

84
Q

Table 36-2 Action of Insulin Preps

A

see pic in phone

85
Q

Short Term Complications

A
  • DKA
  • Hyperglycemic Hyperosmolar Noketotic Syndrome (HHNS)
  • Hyperglycemia
  • Hypoglycemia

You can NOT live with these conditions chronically. They are acute.

86
Q

Normal body pH?

A

7.35-7.45

87
Q

How does glucose end up in the urine?

A

Blood going into nephron is so concentrated that re absorption in the tubules can’t remove everything. Excess is excreted in urine.

88
Q

Osmotic diuretic

A

Substance that attracts water and takes it along into the Urine

Glucose, Na, Asparagus

89
Q

How does body compensate for acidosis?

A

Kussmal breathing to breath off acetone, a Ketone

90
Q

Ketonuria

A

Ketones in the urine

91
Q

Metabolism of fat creates ?

A

Ketones. Acids

92
Q

Ketones excreted in what ways?

A

Via lungs- fruity breath

Via urine- acetonuria or Ketonuria

93
Q

What complication does Ketonuria cause ?

A

Dehydration, E imbalance

94
Q

DKA causes

A
  • Type 1 - no insulin production

- problem w insulin therapy (missed doses, not enough etc)

95
Q

DKA triggers

A 
Infection- UP BG
PNA (pneumonia)
UTI
Stress
ETOH abuse
Drug abuse
MI (myocardial infarction) heart attack
CVA (cerebro vascular accident) stroke
96
Q

???learn level

Na, K, creatinine, BUN, hematocrit, platelets etc

A

.

97
Q

Hyperglycemia leads to ?

A

Polyuria –> dehydration –> tachycardia–> hypotension–>hypovolemic shock

98
Q

Acidosis leads to ?

A

K+ leaving cellS and accumulate in blood –> hyperkalemia –> UP K can lead to heart attack

99
Q

Hyperglycemia and Acidosis can both lead to loss of consciousness and ?

A

Death

100
Q

DKA symptoms

A 
3Ps
Glucosuria
Ketonuria
Acetone breath
Kussmaul respirations
Drowsiness
BG 250-800 mg/dL
Loss consciousness
101
Q

DKA tests

A

BG, Ketone levels
Urine glucose , ketone levels
Blood pH (acidosis) - ABG arterial blood gas

102
Q

DKA Treatment

A
  • IV Fluids
  • Drip: IV Insulin (REGULAR insulin ONLY)
  • Monitor qH BG (finger prick, side less painful than center fingertip)
  • Monitor Elecrolytes (E)
  • ABG for acidosis
103
Q

DKA patient education

A
  • Teach PREVENTION
  • careful SELF/HOME monitoring of BG
  • if BG >250 then check for Ketones
  • If KETONES present, drink H20 and recheck Ketones again w next urination
  • If KETONES present, call MD
  • Never stop Insulin w/out MD supervision
104
Q

STEROIDS increase

A

UP BG levels

105
Q

about HHNS (Hyperosmolar, Hyperglycemic Nonketotic Syndrome)

A

Occurs Primarily in: Type II, Meds (steroids)

Cause: Stress, Illness, Infection, MI, CVA

106
Q

DKA vs HHNS

A

DKA
No insulin
metabolizes fat

HHNK
severe hypoglycemia but no Acidotic state (DKA). No DKA because there is always at least a little insulin present

107
Q

HHNK Pathophisiology. How fast develops?

A
  • Hyperglycemia —> Polyuria —> Dehydration –> a hyperosmolar state (concentrated urine) –> E imbalance
  • Develops slowly
108
Q

HHNK BG levels?

A

> 600-1500 mg/dL

109
Q

HHNK Symptoms

A
  • Extreme Polydypsia
  • Glucosuria
  • 3 Ps
  • Lethargy
  • Confusion
  • Shock
  • coma
  • death

No ketones (no ketonuria)

110
Q

HHNK Treatment

A
  • IV fluids
  • DRIP: IV REGULAR insulin
  • Monitor: qH BG (finger prick)
  • Monitor: E
  • Teach prevention
111
Q

All DM patients should have an Endocrinologist

A

.

112
Q

HHNK Long Term complications

A
  • Cardiovascular Disease
  • Neuropathy
  • Nephropathy
  • Retinopathy
  • Foot damage: blisters, cuts
  • Osteoporosis
113
Q

Hyperglycemia Definition, Cause

A

Def: calories in excess of insulin available for glucose used
Cause: over-eating, stress, illness, LO DM meds (need to be adjusted)

Stress = release of counter regulatory hormones (epi, cortisol, GH, Glucagon)

114
Q

S/S Hyperglycemia

A
  • 3Ps
  • Fatigue
  • Blurred vision
  • Headache
  • Abdominal Pain
115
Q

Hyperglycemia Rx

A
  • BG meter monitoring
  • BG >250 check urine for Ketones
  • sliding insulin scale, oral agents
116
Q

Hypoglycemia Def.

A
  • not enough glucose in relations to Insulin

- BG

117
Q

cause of Hypoglcemia?

A
  • meds
  • malnutrition
  • fasting
  • excercise
118
Q

What’s the danger of repeated hypoglycemic episodes

A
  • Diabetic Coma

- Brain cells deprived of enegy (neuro damage)

119
Q

Hypoglycemic S/S

A
  • hunger
  • sweating
  • palor
  • tremors
  • palpitation
  • headache (h/a)
  • weakness
  • blurred vision
120
Q

as Hypoglycemia progresses…..s/s

A
  • irritability
  • confusion
  • seizures
  • coma
121
Q

Hypoclycemia Rx

A
  • if pt AOO (awake, alert, oriented), NON ACUTE
  • confirm hypoglycemia w Glucometer
  • administer a Fast Sugar, recheck in 15min, if not BG not high enough (~80-120), more fast sugar. End w long acting sugar.
122
Q

Fast Sugar

A
  • 4oz OJ
  • 1 Glucose Tab
  • 6-8 lifesavers
  • 6oz reg soda
123
Q

Long Acting Sugar (complex carb)

A
  • crackers
  • milk
  • peanut butter
  • 1/2 sandwich
124
Q

Hypoglycemia Treatment: If pt not alert or unable to swallow

A

admin SC, IB, IM

  • IVP 50% Dextrose (D50) (admin by RN)
  • recheck BG in 15 min
  • repeat steps until hypoglycemia subsides
125
Q

If hypoglycemic exhibit neuro S/S, administer STAT?

A

D50 (IV)
Glucagon (SubQ)

Treat asap because brain cells dying. If it turns out to NOT be hypoglycemia, you can always correct the condition by administering insulin.

126
Q

Fasting BG Levels (8-12hrs NPO)

A
  • 70 to 99 mg/dL - Normal
  • 100 to 125 mg/dL - Pre DM
  • > 126 mg/dL on more than 1 test occasion - DM
127
Q

Long Term Complications of DM

A
  • Macrovascular
  • Microvascular
  • Nerves
  • Infection
  • Foot Complications
128
Q

MACROvascular Complications

A

Involve circulatory system

  • Atherosclerosis (plaque/narrowing of arteries)
  • Arterioosclerosis (Hardening of arteries)
  • HTN (UP press in vessels, risk for heart attack)
  • UP LDL/Triglycerides
  • Platelet fx - MI/CVA
  • Poor circulation in feet/legs
  • DM alters clotting ability (clotting when not necessary)
129
Q

MICROvascular Complications

A

Eyes

  • Retinopathy (disease of retina. dmg tiny blood vess that supply eye)
  • Cataracts (clouding of lens)
  • Glaucoma (UP press in eyes)

Kidneys
-Nephropathy

130
Q

What % of DM develop cataracts? Glaucoma?

A

60%, Cataracts

40%, Glaucoma

131
Q

Leading cause of blindness

A

Glaucoma

132
Q

Types of Retinopathy

A

Nonproliferative

Proliferative

133
Q

Non Proliferative Retinopathy

A

capillaries in back of eye balloon, form pouches that inhibit passage of substances btwn blood and retina

134
Q

Proliferative Retinopathy

A

blood vessels so damaged they close off. new weak vessels grow in retina, leak blood

135
Q

Nephropathy

A

Disease of kidneys. Blood vessels damaged due to hyperglycemia. Result in ESRD - Dialysis. affect filtering ability

136
Q

Leading cause of ESRD?

A

DM

137
Q

what % of DM px develop nephropathy?

A

40% develop some degree of kidney problems

138
Q

Neuropathy

A

nerve damage from Chronic Hyperglycemia

  • numbness/pain in extremities
  • Gastroparesis
139
Q

Gastroparesis?

A

delayed gastric emptying (paralyzed stomach)

140
Q

MED: REGLAN, 2 uses?

A

Nausea and Gastroparesis

-Increase speed in which contents empty from stomach

141
Q

Complications of INFECTION

A

DM px prone to infection

  • UP BG
  • lead to DKA in Type 1
  • slow healing, impaired circulation. not enough blood getting to would
  • Hyperglycemia -> WBCs sluggish/ineffective. can’t fight infection
  • ulcers/infections -> gangrene, necrosis, death
  • Abx given, but not effective due to poor circulation
  • use TOPICAL Abx
142
Q

what 3 factors lead to Foot Complications?

A
  • poor circulation (vascular disease)
  • prone to infection (poor would healing)
  • neuropathy (limits sensation)
143
Q

leading cause of Amputation?

A

DM

144
Q

Foot Care Steps

A
  • wash and dry feet DAILY
  • Inspect for cracks, sores, foreign objects
  • clip toe nails across, not angle, to avoid ingrown
145
Q

Teaching Footcare. What to AVOID?

A
  • pantyhose, garters, tight socks
  • crossing legs
  • foot soaks/powders
  • lotion btwn toes –> fungal infec.
  • never barefoot
  • hot H2O bottles, heating pads on feet
146
Q

Teaching Footcare. What to DO?

A
  • use alcohol free lotion, NONE btwn toes
  • wear proper shoes, wide, sturdy
  • see podiatrist
  • annual checkups
  • notify MD of abnormalities
147
Q

DM Rx

A
  • education w monitoring
  • diet
  • excercise
  • oral agents
  • Insulin (last resort)
148
Q

Goals of Diet

A

1) achieve/maintain BG and Lipids to near normal (CONTROL to avoid complications)
2) weight loss and BP control / Meal planning

149
Q

3 Methods of Meal planning

A

-Plate method
-carb counting
-glycemic index
(refer pt to nutritionist/dietitian)

150
Q

Benefits/Risk of Excercise

A

UP Muscular activity -> glucose utilization, insulin receptors become more sensitive to insulin

Risk for HYPOglycemia (supervised exercise recommended)

151
Q

Exercise Concerns

A
  • monitor BG before, during, after (to see how BG affected)
  • Gradually UP level of activity
  • Avoid extremes -> Hypoglycemia
  • Excercise SAME time daily. easier to monitor
  • BG 90andUP before exercise (if on oral meds)
  • BG 110andUP before exercise (if on insulin)
152
Q

When Exercise make sure to:

A
  • carry Fast Sugars

- eat carb snacks before and at intervals during strenuous workouts.

153
Q

If on INT acting Insulin, DO NOT exercise during

A

PEAK hours (when BG is lowest)

154
Q

Type1, if BG is 250andUP, what to do before excercise? why?

A

-check for Ketones. If present, DON’T excercise because Ketones will increase. Body will start metabolizing fat after all glucose is done.

  • Drink H2O, check urine again
  • H2O to prevent dehydration because Glucose and Ketones in urine are Osmolor diuretics.
155
Q

Excercise - pre-workout list

A
  • Med alert ID
  • Comfy shoes (prevent blisters)
  • bring glucometer
  • carry fast sugar
  • bring emerg glucagon kit
156
Q

If BG is 300andBLO, no ketones present, can you exercise?

A

yes

157
Q

Exercise if Type II, if BG 400andBLO?

A

YES

158
Q

Exercise if Type II, if BG 400andUP?

A

NO

159
Q

BG monitoring

A
  • self monitoring
  • take daily log w times, #s
  • Tight glucose control - qac and qhs (b4 meals and bedtime)
160
Q

??? Glucosuria when BG is ?

A

> 80 mg/dL

161
Q

Test urine for ketones when ?

A

> 250 mg/dL

Type II don’t check for ketones because they always make insulin

162
Q

MEDS: 6 class of Oran HYPOglycemics

A

1) Sulfonylureas
2) Meglitinides
3) Alpha-glucosidase inhibitors
4) Thiazolidinediones
5) Biguanide
6) DPP-4 Inhibitors

163
Q

Ca and K for?

A

Ca - relieves contracting Muscles

K - relaxing muscles (too much, risk for MI)

164
Q

MEDS: Sulfonylureas - how do they work?

Type II DM

A
  • stimulate pancreas to release more insulin
  • NOT dependent on BG
  • can –> HYPOglycemia (monitor BG because of this)
  • NEVER use on Type 1 (IDDM)
165
Q

MEDS: Sulfonylureas - examples

A

1st gen:
Diavinese

2nd gen:
Glipizide (Glucotrol)
Glyburide (Diabeta, Micronase, Glynase)

3rd gen:
Glimepiride (Amaryl)

SIDE EFFECTS: Nausea, Diarrhea, Constipation

166
Q

MED: Diavinese

A
  • 1st Gen Sulfonylurea

- not used often. stress on kidney. Renal function can be altered

167
Q

MED: Glipizide (Glucotrol)

A
  • 2nd gen Sulfonylurea
  • given 30 min B4 1st meal, breakfast

SE: Nausea, Diar, Constip

168
Q

MED: Glyburide (Diabeta, Micronase, Glynase)

A
  • 2nd gen Sulfonylurea
  • given 1x day w 1st meal

SE: Nausea, Diar, Constip

169
Q

MED: Glimepiride (Amaryl)

A
  • 3rd gen Sulfonylurea
  • 1x day w 1st meal

SE: Nausea, Diar, Constip

170
Q

MEDS: Meglitinides - how do they work?

A
  • stim pancreas to release insulin
  • Glucose DEPENDENT
  • Taken 30min B4 meal

once pt eats, UP BG, then pancreas w stim insulin. absorption happens in sm intestines. Med will already be working

171
Q

MED: Meglitinides - examples

A
  • Prandin (Repaglinide)
  • Starlix (Nateglinide)
  • stim pancreas to release insulin
  • Glucose DEPENDENT
  • Taken 30min B4 meal
172
Q

MED: Alpha-glucosidase Inhibitors - how do they work?

A
  • prolong absorption of carbs in stomach & intestines. BLOCKS enzyme needed to digest starch.
  • slows post prandial, UP BG
  • given w EACH meal on 1st bite, not convenient
173
Q

MED: Alpha-glucosidase Inhibitors - i.e.

A

Precose (Acarbose)

not convenient because have to remember for each meal.

174
Q

MED: Precose (Acarbose)

A

w EACH meal on 1st bite.

175
Q

MED: Thiazolidinediones - how do they work? (like Biguanides)

A

-UP insulin sensitivity at insulin receptors
-LO amount of glucose released by liver
-taken daily w NO regard to meals
-similar to Biguanide’s
UP risk/rate of bladder CA. Contraindicated in pts w Hx of Bladder CA

176
Q

MED: Thiazolidinediones - i.e.

A

Avandia (risk for MI) not used anymore
Actos (Pioglitizone)

  • UP insulin sensitivity at insulin receptors
  • LO amount of glucose released by liver
  • taken daily w NO regard to meals
177
Q

MED: Actos (Pioglitizone) class

A

Thiazolidinedione

  • UP insulin sensitivity at insulin receptors
  • LO amount of glucose released by liver
  • taken daily w NO regard to meals
178
Q

MED: Biguanide -(2 uses, Bi) how does it work?

A
  • used in combo w Sulfonylureas
  • LO hepatic glucose output
  • UP insulin sensitivity at cell. so don’t need as much
  • taken w 1st meal, 1x day
  • DOES NOT cause HYPOglycemia because it doesn’t raise insulin. only makes insulin already there more effective.
  • RISK hepatotoxicity. don’t use on pts using contrast mediums because dyes are nephrotoxic. drug already hard on kidneys
179
Q

MED: Metformin (Glucophage) class

A

Biguanide

  • taken w 1st meal, 1x day
  • DOES NOT cause HYPOglycemia because it doesn’t raise insulin. only makes insulin already there more effective.
  • used in combo w Sulfonylureas
  • LO hepatic glucose output
  • UP insulin sensitivity at cell. so don’t need as much
180
Q

MED: DPP-4 Inhibitors aka (Gliptins) - how do they work?

A
  • hormone in GI tract sign pancreas to produce insulin
  • glucagon like polypeptide 1 (GLP-1)
  • DPP-4 is protein found in blood. it stops breakdown of diff hormones to UP insulin to LOWER BG.
  • short acting in blood
  • taken w/out regard to food
  • Only for Type II, dependent on insulin releasing cells

i.e. Januvia

181
Q

MED: Januvia class

A

Gliptin (DPP-4 Inhibitor)

-taken w/out regard to food. anytime

182
Q

MED: Glucagon

A
  • converts Glycogen to Glucose
  • Emergency med
  • UP BG levels
  • Rx for unconsios pt (subQ, IV, IM, parenteral)
  • must be constituted STAT before injection
  • RISK for bleeding with pts on Cumadin
183
Q

Evidence of internal bleeding?

A
  • urine in blood
  • bruising
  • bleeding mouth
184
Q

Insulin pump

A
  • CSII - Continuous SubQ Insulin infusion (mimics pancreas)
  • Batter powered computer device
  • Admin a BASAL rate or a BOLUS rate

GOAL: keep BG steady btwn meals and at night

185
Q

Insulin made of

A

Human or Pork

-if you don’t know what type of insulin pnt uses, use Human

186
Q

Types of Insulin

A

Rapid, short, inter, long acting

187
Q

What type of Insulin can you mix?

A

All but Lantus (Long Acting)

188
Q

Where to store insulin?

A

in fridge. Avoid Extreme temp and agitation.

Discard after 1 mos. and if has precipitate, lumpy, frosted.

189
Q

Safe use of pump requires?

A
  • committed to checking BG at lease qID (4x day)
  • CHO counting method
  • adjust Insulin based on BG levels, CHO and physical activity
190
Q

Pump Advantages

A
  • flexibility in lifestyle
  • predictable insulin delivery
  • precise insulin deliver
  • accurate deliver (up to 1/10th unit) human eye can only see 1u.
  • LO episodes of HYPOglycemia
  • LO fluctuations in BG
  • helps manage Dawn Phenomenon
191
Q

Pump Disadvantages

A
  • risk of skin infections
  • risk of DKA from pump malfunction
  • cost
  • lets other know you have DM (?)
192
Q

Good sites for Insulin inj.

A

fleshy parts

  • Abdomen
  • back of arm where you can bunch skin
  • 45* subq, if can bunch more than 1”, 90*
  • needle bevel up
  • only RN can administer
193
Q

Somogyi effect

A

rebounding high blood sugar that is a response to low blood sugar.

194
Q

Dawn Phenomenon/Dawn Effect,

A

abnormal early-morning increase in blood sugar (glucose) — usually between 2 and 8 a.m. — in people with diabetes.

Nursing, LPN, Year 2 (27 decks)

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