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Nursing, LPN, Year 2 > X Diabetes Mellitus Quiz/HW > Flashcards

X Diabetes Mellitus Quiz/HW Flashcards

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1
Q

DM defined as…

A

a group of systemic metabolic disorders characterized by hyperglycemia

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2
Q

DM cannot be…

A

cured

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3
Q

How can DM pt reduce complications?

A

diet, excercise

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4
Q

list 4 types of DM

A
  • Type 1 (IDDM)
  • Type 2 (NIDDM)
  • Gestational DM
  • Other
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5
Q

?Define Pre-DM

A

BG abnormal (100-126 mg/dL) but not meeting criteria for DM which is (?) >200mg/dL (? after fasting overnight)

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6
Q

Juvenille DM knows as

A

Type 1, Insulin Dependent DM (IDDM)

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7
Q

Adult onset DM aka

A

Type II, Non Insulin Dependent DM (NIDDM)

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8
Q

What is most prevalent type of DM?

A

Type II, NIDDM

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9
Q

list 5 factors assoc. w development of Type II DM

A
  • poor diet
  • sedentary lifestyle
  • obesity
  • race
  • age
  • family history
  • Hx of gestational DM
  • ETOH abuse
  • smoking
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10
Q

List 4 Modifiable risk factors

A

Diet, excercise, obesity, smoking

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11
Q

List 4 NON modifiable risk factors

A

Race/Ethnicity, Age, Family History, Gestational DM

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12
Q

Majority of Type II DM are…

A

obese

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13
Q

People w DM at hi risk of dev…..

A

stroke, heart disease

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14
Q

? DM leading cause of …

A
  • ESRD, End Stage Renal Disease

- Blindness (?)

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15
Q

DM is ? leading cause of ?

A

7th, Death

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16
Q

what are hi risk populations for dev DM?

A

-African Am
-Asian Am
-Native Am
-Pacific Islanders
-Latino
(anything w American)

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17
Q

Viruses that trigger DM, Type 1

A
  • Mumbs/Rubella

- Coxsackie 4

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18
Q

Relationship btwn GLUCOSE and INSULIN

A

Lock and key

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19
Q

Insulin is a ? produced by the ?

A

Hormone, Beta Cells in the Islets of Langherhan of the Pancreas

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20
Q

Stimulus for Insulin production is ?

A

UP BG (hyperglycemia)

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21
Q

? Routing screening for DM should be done on anyone with 1 or more of the ? risk criteria?

A

Non Modifiable and Modifiable
-HTN
-Impaired Glucose Intolerance
? -HDL 250

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22
Q

List 3 tests used to screen for DM

A
  • A1c
  • OGTT (>200mg/dL)
  • Fasting BG (>126mg/dL)
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23
Q

Definition of Glucosuria

A

glucose present in urine.

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24
Q

Polydipsia

A

excessive thirst

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25
Q

Polyuria

A

excessive urination

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26
Q

Polyuria results in…

A

dehydration. glucose is an osmotic diuretic

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27
Q

Polyphagia

A

excessive eating

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28
Q

Lantus?

A

Long Acting Insulin

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29
Q

Which insulin faster acting and why?

HumalinR or Humalog

A

Humalog is faster acting.

Humalog is RAPID acting and onset only 15min. HumalinR is Fast Acting w onset of 30min - 1hr.

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30
Q

List an intermediate acting insulin

A

NPH (NovolinN, HumulinN)

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31
Q

Type I DM produce ? insulin?
What cells are damaged?
Type I are insulin ?

A
  • NO insulin
  • Beta cells from Islets of Langerhans
  • Insulin Dependent (IDDM)
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32
Q

3 symptoms of Type 1

A

3 Ps (polyuria, polydypsia, polyphagia)

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33
Q

Classic symptoms of DM

A

3 Ps (polyuria, polydypsia, polyphagia)

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34
Q

problem w Type 2 DM is insulin ? , rather than lack of insulin

A

Resistance

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35
Q

Decreased sensitivity to Insulin known as insulin ?

A

resistance

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36
Q

Insulin attaches to insulin cell X and allows X to leave X to enter cell

A

receptors, glucose, blood stream

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37
Q

Glycogen is

A

storage form of glucose (liver, (muscle, adipose))

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38
Q

Glucagon is

A

hormone released by pancrease to UP BG. breaks down glycogen to form glucose to be used as energy

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39
Q

Glucose is

A

mono-saccharide, simple sugar

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40
Q

HUMALOG
REGULAR
NPH
LANTUS

A

HUMALOG, Rapid Act, 15min, 30 - 1hr PEAK, 3-6.5hr DURATION

REGULAR, Short Act, 30-1hr, 2-3hr PEAK, 4-6hr DURATION

NPH, Inter Act, 1-2hr, 6-14hr PEAK, 16-24hr DURATION

LANTUS, Long Act, 2hr, NO PEAK, 24hr DURATION

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41
Q

Who most at risk for dev DM?

Caucasian woman, Asian woman, AfAm woman, hispanic child?

A

AfAm

anyone w american

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42
Q

risks for dev of DM?

Over 45
overweight
HDL >40md/dL
Sendentary lifestyle

A

YES Over 45
YES overweight
NO HDL >40md/dL (concern is

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43
Q

Normal fasting GL

A

99mg/dL and below

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44
Q

prep for fasting BG

A

-NPO 8hrs

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45
Q

normal post prandial BG

A
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46
Q

normal pre prandial BG

A

99mg/dL and below

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47
Q

Poorly controlled DM will have hba1c of

A

9%

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48
Q

what w serum insulin show in NIDDM and why?

A

how much insulin being produced and how well the body is using it. Normal to hi if NIDDM under good control, HI if becoming resistant

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49
Q

What w serum insulin show in IDDM and why?

A

no insulin present in IDDM showing that body is not producing any.

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50
Q

How will C-peptide show person is Facticiously Hypoglycemic?

A

one C-Peptide produced per Insulin . If the two numbers don’t match, you can determine over dose of insulin in order to lower BG.

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51
Q

Incidence of complications are ? in IDDM and ? in NIDDM?

A

frequent in both

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52
Q

What is glucose?

A

Simple sugar, monosacharide

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53
Q

Stored glucose is ?

A

glycogen

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54
Q

? is released from pancreas and instructs liver to convert ? to glucose?

A

Glucagon, Glycogen to Glucose

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55
Q

If body cannot use glucose for energy, it will use ? instead. this creates by products called ?. List them….

A

fat. ketones.

AAH….
Acetone, Acetoacetic Acid, Hydroxybutyric Acid

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56
Q

List 6 causes of insulin resistance

A

obesity, hereditary, sedentary lifestyle, age, diet, race, metabolic syndrome, steroids, meds

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57
Q

Type I DM usually develops at age ?

A

40 and below

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58
Q

Type II DM usually develops?

A

40 and older

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59
Q

Why is gestational DM a concern?

A

can increase risk for patient to develop NIDDM in future pregnancies. Risk for baby to be hypoglycemic due to overproduction of insulin.

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60
Q

Glycosuria

A

excess glucose in urine

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61
Q

Hirtsutism

A

male pattern hair growth in women

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62
Q

8 S/S of DM

A

3Ps, slow wound healing, halos, blurred vision, cold extremities, nausea, impotence, neuropathy

63
Q

Hypoglycemia BG levels

A
64
Q

Normal values

  • A1c
  • Pre Prandial
  • Post prandial
  • Serum Insulin
A
  • A1c - 5% and below
  • Pre Prandial - 100 mg/dL and below
  • Post prandial - 140 mg/dL and below
  • Serum Insulin - 5-24 mcU/L
65
Q

Ketones are toxic ?

A

Acids

66
Q

Ketones mainly produced in pt w TYPE?

A

Type I

67
Q

Type 2 DM develop this complication

A

HHNS (Hyperosmolar, Hyperglycemic, Nonketotic Syndrome)

68
Q

Components of good or tight glycemic control

A

A1c test under 5%. overall sense of wellbeing, normal BP (130/80)

69
Q

? Why does DKA lead to metabolic acidosis

A

build up of ketones creates acidotic body affecting metabolism.

70
Q

DKA characterized by….

A

vomiting, kussmaul breathing, confusion, dehydration

71
Q

2 causes of DKA

A

IDDM, starvation, fasting

72
Q

3 triggers of DKA

A

hyperglycemia, stress, starvation, no insulin

73
Q

How does body compensate for acidic state of DKA

A

Kussmaul breathing

74
Q

DKA will occur in BG of

A

> 250 mg/dL

75
Q

SS of DKA

A

poor skin turgor, BG >250, dry mouth, fruity breath, tired, confusion, 3ps, nausea

76
Q

what is Rx for DKA?

A

Ingest Insulin, IV Therapy, Meds, Electrolytes

77
Q

what type of Insulin administered during DKA?

A

REGULAR, IV

78
Q

Why doesn’t DKA develop in NIDDM?

A

because there is always insulin present so body never metabolizes fat.

79
Q

what is osmotic diureses?

A

UP urine due to certain substances in urine acting as osmolor diuretics. Osmolar Hyperglycemic state

80
Q

HHS characterized by?

A

Hyperglycemic, Hyperosmolality and dehydration without ketoacidosis. Change in level of consiousness

81
Q

P.925

5 SS of HHNS

A
  • BG>600mg/dL
  • dry mouth
  • polydypsia
  • fever over 101
  • loss of vision
  • hallucinations
  • weakness on 1 side body
82
Q

5 SS of hypoglycemia

A

-confusion, weakness, shakiness, anxiety, heart palpitation

83
Q

Ketosis present in ?? and not in ??

A

DKA, not in HHNS

84
Q

list 4 rapid acting sugars

A

lifesavers, soda, oj, raisins

85
Q

15/15 rule

A

test BG, give 15g fast acting sugar, wait 15 min, retest and give again. repeat until levels normal.

86
Q

Somogyi effect

A

when body reacts to night time hypoglycemia, stimulating glucagon, leaving pt hyperglycemic in the am.

87
Q

Rx for Somogyi effect

A

treat hypoglycemia in timely manner, lower eve dose of insulin

88
Q

cause of Dawn Phonomenon

A

Body produces hormones to raise BG. 4-8am. no carbs at night, adjust night insulin

89
Q

Insulin administered w ??

A

Insulin syringe only

90
Q

what type of insulin administered via IV?

A

REGULAR only

91
Q

What type of insulin can be administered thru insulin pump?

A

Rapid Acting or Regular

92
Q

What can Lantus be mixed with?

A

NOTHING

93
Q

Insulin introduced as Rx when ?

A

Diet, Exercise or meds not effective. Insulin in a last resort.

94
Q

LANTUS
REGULAR
HUMALOG
NPH

A

LANTUS, Long act, 2hr, NO PEAK, 24hr DURATION

REGULAR, Short Act, 30min - 1hr, 2-3hr PEAK, 4-6hr DURATION

HUMALOG, Rapid act, 15min, 30-2.5hr PEAK, 3-6.5hr DURATION

NPH, Interm Act, 30min, 4-8hr PEAK, 24hr DURATION

95
Q

3 causes of hypoglycemia

A
  • med
  • excercise
  • malnutrition
  • fasting
  • insulin OD
  • unplanned strenuous activities
96
Q

If pt has BG of 35, what symptoms w they experience?

A
  • irritability
  • hunger
  • sweating
  • palor
  • tremors
  • palpitation
  • tachycardia
  • muscle weakness
  • coma
  • polyphasia
  • blurred vision
  • headache
97
Q

Treatment for unresponsive DM in hypoglycemic state?

A

-IV,SubQ, IM, Glocagon, D50

98
Q

HHNS

A

Hyperosmolar, Hyperglycemic, NonKetotic Syndrome

99
Q

HHNS occurs in what type DM?

A

Type II, NIDDM

100
Q

BG in HHNKS can be as high as?

A

1500 mg/dL

101
Q

HHNKS diff from DKA how?

A

in HHNKS, small amount of insulin prevents ketosis and acidosis

102
Q

??4 things that precipitate HHNS

A

MEDS, steroids, Thiazidoliniese, Dilantin?, acute illness, infection, trauma

103
Q

5 causes of DKA

A
  • lack of insulin
  • med mistakes
  • infection
  • ETOH/Drug abuse
  • CVA
  • MI
  • PNA
  • UTI
  • Stress
  • pump failure
  • non compliance
104
Q

DKA info

A

An infection or other illness can cause your body to produce higher levels of certain hormones, such as adrenaline or cortisol. Unfortunately, these hormones counter the effect of insulin — sometimes triggering an episode of diabetic ketoacidosis. Pneumonia and urinary tract infections are common culprits.

105
Q

DKA info

A

Diabetic ketoacidosis occurs when a person with diabetes becomes dehydrated. As the body produces a stress response, hormones (unopposed by insulin due to the insulin deficiency) begin to break down muscle, fat, and liver cells into glucose (sugar) and fatty acids for use as fuel.

106
Q

In DKA, fruity breath comes from

A

Acetone, excreted by Lungs

107
Q

Rx for DKA

A

IV Regular Insulin, fluids, monitor E, monitor BG

108
Q

Untreated DKA –>

A

coma, death

109
Q

Untreated hypoglycemia –>

A

coma, death

110
Q

DM should inspect feet how often?

A

daily

111
Q

If severely sick, monitor BG how often?

A

q2hrs

112
Q

instruction for DM pt travelling

A

-extra supplies, insulin, needles, batteries, fast sugar, emergency glucagon kit, medic alert bracelet, planned meals, H2O q2 hrs

113
Q

rebound hyperglycemia

A

Somogyi effect - high blood sugar that is a response to low blood sugar.

114
Q

Dawn Phenomenon

A

a normal rise in blood sugar as a person’s body prepares to wake up.

In early am, hormones cause the liver to release large amounts of sugar into bloodstream. body produces insulin to control rise in blood sugar.
If body doesn’t produce enough insulin, blood sugar levels can rise. This may cause high blood sugar in the morning (before eating).

115
Q

4 LT complications of DM

A
  • microvascular (eyes:glaucoma, retinopahty, cataracts)
  • macrovascular (atherosclerosis)
  • neuropathy (nerves)
  • nephropathy (kidney)
116
Q

test for acetone when BG at what level?

A

> 240 mg/dL

117
Q

nephropathy

A

damage to blood vessels in kidney

118
Q

how many develop some sort of Nephropathy?

A

40% DM pts

119
Q

Albuminuria

A

protein in urine

120
Q

Most common visual problem in DM

A
  • glaucoma
  • retinopathy
  • cataracts
121
Q

what can help preserve vision?

A

frequent eye exams, tight glucose control

122
Q

Gastroparesis

A

delayed gastric dumping, caused by damage to vagus nerve, which regulates the digestive system

123
Q

Gastroparesis associated w

A

neuropathy

124
Q

what cardiovascular disease are DM risk for?

A

Atherosclerosis

125
Q

2/3 ppl w DM die of ? and ?

A

stroke and heart attack (MI, CVA)

126
Q

Lines of treatment for DM

A

1) diet, excercise
2) oral meds
3) insulin (last resort)

127
Q

chronic hyperglycemia –>

A

blood vessels, nerve, kidney

128
Q

diabetic nephropathy –>

A

ESRD

129
Q

(?) normal BG level is

A

70-130 (DONT AGREE)

130
Q

Hypoglycemia is

A
131
Q

Hyperglycemia is

A

Fasting > 130 mg/dL

Postprandial > 180 mg/dL

132
Q

Humalog

A

rapid acting

133
Q

Regular Insuling

A

Short (fast) acting

134
Q

Lantus

A

Long acting

135
Q

Which is a Sulfonylurea?

Metformin, Actos, Precose, Glucotrol?

A

Glucotrol

136
Q

how do Sulfonylureas work?

A

stimulate pancreas to release insulin. NOT dependent on BG

137
Q

How do Biguanides work?

A
  • LO hepatic glucose output
  • UP insulin sensitivity at cell. so don’t need as much

-DOES NOT cause HYPOglycemia because it doesn’t raise insulin. only makes insulin already there more effective.

138
Q

How do Thiazolidinediones work?

A

-UP insulin sensitivity at insulin receptors
-LO amount of glucose released by liver
-taken daily w NO regard to meals
(similar to Biguanides)

139
Q

How do Alpha-Glucosidases 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
140
Q

How do Meglitinides work?

A
  • stim pancreas to release insulin
  • Glucose DEPENDENT
  • Taken 30min B4 meal
141
Q

Metformin is what class? Trade Name?

A

Biguanide. Glucophage

-DOES NOT cause HYPOglycemia because it doesn’t raise insulin. only makes insulin already there more effective.

142
Q

Glipizide is what class? Trade Name?

A

Sulfonylurea. Glucotrol.

143
Q

Metformin given when?

A

w 1st bite

teach says w or shortly after. (WRONG?)

144
Q

Glipizide taken when?

A
  • 30 min before meal.

- Sulfonylurea

145
Q

Glyburide class? administered when?

A

Sulyfonylurea, w 1st meal.

146
Q

Prandin class? administered when?

A

Meglinitinide, 30 min b4 meal

  • stim pancreas to release insulin
  • Glucose DEPENDENT
  • Taken 30min B4 meal
147
Q

Precose class? administered when?

A

Alpha-Glucosidase, w 1st bite of meal.

  • 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
148
Q

Actos class? administered when?

A

Thiazolidinedione

-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

149
Q

Lantus administered ?

A

same time each day

150
Q

DM is syndrome characterized by?

A

Hyperglycemia

151
Q

DM due to damage to ?

A

Beta cells in pancreas, affecting producton and release of insulin

152
Q

Type I DM cause?

A

Autoimmune

153
Q

Type II DM cause?

A

obesity

154
Q

What DM will resolve itself?

A

Gestational DM

Nursing, LPN, Year 2 (27 decks)

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