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202D > Test#2 > Flashcards

Test#2 Flashcards

1
Q

What are the vitamin k dependent clotting factors

A

8 9 10 prothrombin(2)

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2
Q

What clotting factors does heparin act on

A

Xa

IIa

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3
Q

What allergy would indicate the pt will have a possible allergic reaction to heparin

A

An allergy to enoxapain or pork

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4
Q

What clotting factor does enoxaparin work on

A

Xa

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5
Q

what form is does heparin come in

A

IV and Sub Q

-you don’t want to give it IM b/c you will cause a hematoma

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6
Q

what is heparin derived from

A

mucosal tissue of animals.

beef lung and pig intestines.

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7
Q

what does heparin do

A

inhibits the activity of coagulation factors Xa and IIa to prevent clot from forming.
-it prevents the enlarging of existing clots and prevents new ones.

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8
Q

what is enoxaparin

A

a low molecular weight heparin

-it is cut up into smaller fragments of heparin which makes it less effective

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9
Q

what clotting factors does enoxaparin inhibit

A

Xa

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10
Q

what is anti-thrombin III

A

a protein in the blood stream
-a natural anticoagulant that prevents us from forming unnecessary clots.. it inhibits clotting factors along the cascade including thrombin

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11
Q

what is the relationship between anti-thrombin III and heparin

A

anti-thrombin binds to heparin and it forms a complex that makes the heparin 1000x more effective and inhibiting Xa and IIa

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12
Q

what is the relationship between anti-thrombin III and Enoxaparin

A

it binds to enoxaparin and forms a complex but creates a shorter chain therefore allowing it to only block factor Xa

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13
Q

what is the indication for heparin

A

-prophylaxis and tx of thromboembolic events.

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14
Q

what pts are at high risk for thromboembolic events

A 
a-fib
surgery pts
HTN 
bedridden
CAD
pts who have multiple risk factors.

also in small doses in pediatric unit to keep peripheral IV lines open.

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15
Q

with what med is heparin used with and why

A

warfarin
because warfarin has such a long onset of action and heparin is fast, heparin is given as a “bridge therapy” until warfarin’s reaches its therapeutic level

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16
Q

How is heparin given if its given prophylactically

A

via a subQ injection Q8-12hours

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17
Q

what needs to be monitored with heparin when given propylactically

A

nothing. No monitoring of labs etc is needed when heparin is given prophylactically.

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18
Q

how long is warfarin onset of action

A

36-72hours

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19
Q

how is heparin given if it is being used for treatment of clots

A

It is given IV

-it depends on the clot and what they are being treated for to decide whether it is intermittent or continuous

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20
Q

what is standard practice when administering heparin initially for treatment

A

Administering a loading dose.(AKA loading bolus)
given first via IV or injection
then followed by intermittent or continuous IV therapy

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21
Q

why is a heparin loading dose given

A

to get to the therapeutic level faster

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22
Q

how do we monitor if the patient is in the therapeutic level of heparin

A

by assessing the PTT levels

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23
Q

what is PTT and what is it for

A

Partial Thromboplastin time.
it measures the time in seconds how long it takes for a clot to form.
it is ONLY used for heparin monitoring.

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24
Q

what is the therapeutic range for heparin

A

1.5-2.5 times the control

control depends on facility

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25
Q

what do you need to do prior to administering an intermittent infusion of heparin

A

collect a PTT 30 minutes prior to initial dose to obtain baseline

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26
Q

what is heparins half life

A

1-2hours

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27
Q

how often is PTT monitored when giving a continuous infusion of heparin

A

Q4-6Hours

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28
Q

what should you do if the PTT is critically high

A

stop the infusion for 1 hour and then redraw a PTT.

consult with the pharmacy to let them know and see what their recommendation is.

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29
Q

what is HIT

A

Heparin induced thrombocytopenia

it is a side effect of heparin therapy

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30
Q

what causes HIT and how does it happen

A

it is an immune induced response in which the body creates antibodies to platelets.
the platelets release PF4 and it binds to heparin- which then binds to antibodies creating a complex that attaches to the platelet at the receptor (this causes macrophages to clean them out{loss of platelet} and induction of tissue factor-leading to clot.)

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31
Q

what is the normal platelet range

A

150,000-450,000

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32
Q

when would you begin to notice HIT and what will you notice.

A

it will develop around the 8th day of therapy.

  • the platelet amount will drop approx 50% drop
  • s/s of thrombi formation
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33
Q

what do you do if HIT occurs

A

stop therapy immediately, notify the dr and alternative anti-coagulants can be administered.

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34
Q

what is enoxaparin used for

A

prophylaxis and treatment of DVT/PE

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35
Q

what would you see enoxaparin be used for

A

post hip, knee, abdomen surgeries

or pts who are bed ridden

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36
Q

what should you look at prior to giving enoxaparin

A

the platelet baseline

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37
Q

what is enoxaparins half life and duration of action

A

4-5 hours 1/2 life and

12 hours duration

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38
Q

what is prophylactic dosage for enoxaparin

A

30-40mg Qday or Q12H

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39
Q

what is the dosage for treatment of enoxaparin

A

1mg/kg q12h
or
1.5mg/kg q24h

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40
Q

what is the difference in dosages from prophylactic and treatment with enoxaparin

A

the treatment for coagulation is based on the patients weight.

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41
Q

what is contraindicated when giving heparin

A

someone who has hemorrhagic stroke and uncontrolled HTN

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42
Q

what is the antidote for heparin

A

protamine sulfate IV form

it inactivates heparin

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43
Q

what are the drug drug interactions with heparin

A
  • sulfa drugs
  • 2nd generation cephalosporins (cefelexin & cefotetan)
  • NSAIDS
  • aspirin
  • Clopidogrel (plavix)
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44
Q

what herbal products interact with heparin

A

the 5 G’s

ginko, ginsing, garlic, green tea, ginger

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45
Q

how does a virus survive

A

it needs to replicate inside the host cell. they fuse themselves to the outer membrane and enter the cytoplasm of the cell and begin replication.
once it has what it needs from one cell, it spreads and attacks other cells

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46
Q

what are the responses to viral infections

A

-non specific:
cell mediated immunity- macrophages
-specific:
humoral immunity

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47
Q

what is cell mediated immunity

A

-neutrophils, macrophages respond and perform phagocytosis
l-ymphocytes release cytokines which stimulate the immune response
-release of b & t cells

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48
Q

what is humoral immunity

A

specific repsonse

the production of antibodies that can attack and destroy viruses.

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49
Q

what are the stages of a viral infection

A
  1. virus attaches to a cell
  2. virus penetrates cell membrane and injects DNA/RNA into cell
  3. viral dna/rna replicates using host cell machinery
  4. new viral dna/rna are packaged into viral particles and released from the host cell
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50
Q

how is herpes aquired

A

through physical contact with an infected person.

the fluid that is within the sores.

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51
Q

where does herpes stay dormant

A

in a non replicating state in the sensory or autonomic nerve root ganglia

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52
Q

what can cause herpes to replicate

A

immunosuppression, medication therapy, medical condition, stressors

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53
Q

what is the cure for herpes virus

A

there is no cure.

there are only medications that can treat the symptoms and reduce the number of outbreaks.

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54
Q

what are the 3 types of herpes

A

herpes simplex virus (HSV)- cold sores/fever blisters
HSV-2- genital herpes
HSV-3- varicella zoster & herpes zoster (chicken pox & shingles)

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55
Q

can genital herpes be transmitted when infected person does not have visible sores?

A

yes

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56
Q

what precautions are worn when around chickenpox

A

contact, airborne and droplet

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57
Q

how is chicken pox transmitted

A
  • *it is highly contagious**
  • contact with blister
  • aerosolized via particles
  • coughing/sneezing
  • touching contaminated items
  • transmitted 1-2 days prior to outbreak or rash
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58
Q

when is chicken pox no longer contagious

A

when the blisters are dry and crusted

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59
Q

who can acquire shingles

A

whoever had chicken pox and has the dormant varicella zoster virus living in their nervous system

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60
Q

is shingles contagious

A

no, you cannot give someone shingles HOWEVER you CAN give someone chicken pox if they’ve never had chicken pox

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61
Q

who is shingles common in

A

ppl who are older than 50

ppl on immunosuppressants

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62
Q

what are s/s of shingles

A

painful blister rash that can last for 2-4 weeks
-rash usually in the trunk area in a diagonal fashion
across the torso and back.

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63
Q

when can a person give shingles to others

A

only contagious when the blisters appear.

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64
Q

what can occur in someone with a hx of shingles

A

they can suffer from post-herpetic neuralgia even after the rash has disappeared.
- aches, burns, stabbing pain, sensitive to touch and numbness
can last months to years

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65
Q

what is disseminated zoster

A

when shingles crosses the midline to other areas of the body. usually appears in immunocompromised system.
this kind of disseminated zoster can shed causing the area to be covered.

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66
Q

where does herpes zoster live

A

in the dorsal root ganglia

when it is reactivated the virus causes shingles.

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67
Q

how do anti viral works

A

directly stop the virus from the replication process by entering the cell the same way the virus does.

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68
Q

what is the purpose of anti virals

A

to try to suppress or eliminate viral activity

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69
Q

what forms does acyclovir come in

A

PO
buccal
IV
topical

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70
Q

what is acyclovir used for

A

HSV 1&2

varicella zoster and herpes zoster

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71
Q

how does acyclovir work against viral infections

A

interferes with viral DNA synthesis and inhibits viral replication
abd reduces the time for healing of the lesions

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72
Q

what are side effects of acyclovir

A

because 90% of the drug goes through the kidneys unchanged being toxic to the kidneys
-Causes
crystalluria- drug has ability to crystalize in the tubules causing renal damage.
Steven-johnson syndrome- painful red purple rash that can blister and shed skin

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73
Q

what nursing interventions should you do when pt is on acyclovir

A

Encourage Hydration to keep crystalluria from forming
monitor kidney function - BUN Creatinine
color of urine- check hydration

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74
Q

what is the purpose for taking acyclovir

A

It will not cure but it will

  • decrease the amount of time the lesions need to heal
  • decrease the severity
  • reduce the amount of recurrence
  • help pain management
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75
Q

what are 2 flu medications

A

Oseltamivir
and
Zanamivir

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76
Q

what are the 2 flu medications effective against

A

influenza A & B

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77
Q

what should you avoid if you have received the flu shot

A

you should avoid taking oseltamivir and zanamivir 2 days prior to getting the flu vaccine or wait 2 weeks after getting the vaccine

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78
Q

what does neuraminidase enzyme do

A

enables viral particles to escape from infected cells to go infect other cells

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79
Q

what does oseltamivir and zanamivir do

A

inhibits neuraminidase enzyme to prevent the infection of other cells

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80
Q

what is zanamivir and what is it used for

A

a powder form inhaler used for the tx or prophylactic flu-related symptoms

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81
Q

when should someone take oseltamivir and zanamivir

A

take within 2 days of exposure.

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82
Q

what can oseltamivir cause in relation to the flu vaccine

A

may decrease the effects of the flu vaccine

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83
Q

what is candida and where is it normally found

A

a type of fungus that normally lives on skin and mucous membranes
normal part of flora on our skin, mouth and urogenital tract

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84
Q

what can an overgrowth of candida cause

A

superficial and systemic infections
overgrowth in the mouth can cause thrush
in the genital tract- yeast infections
on the feet- athletes foot

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85
Q

what can a candida infection be caused from

A

from antibiotic use b/c abx kill infected cells along with normal flora so the fungus has the opportunity to overgrow.
or can be caused from immunosuppressant therapy

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86
Q

what does thrush look like

A

red, white colored patches in the mouth that are slightly raised.
under tongue, back of throat,
can cause difficulty swallowing

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87
Q

what are possible systemic infections of fungus caused from

A

histoplasmosis
aspergillosis
coccidiomycosis

88
Q

who is more likely at risk for systemic fungal infections

A

immunocompromised pts
immunosuppressive pts
pts who are taking anti-rejection drugs

89
Q

how long does it take to treat a fungal infection

A

they are difficult to treat

can take weeks to months

90
Q

what is the most anti fungal medication

A

nystatin

91
Q

how does nystatin work

A

disrupts fungal cell wall membrane
by binding to steriles on the fungal cell membrane
which allows the contents of the fungal cell to leak out.

92
Q

what forms does nystatin come in

A 
lozenge
suspension
tablet
ointment
powder
93
Q

what are the directions for taking a nystatin lozenge

A

it needs to dissolve orally

do not chew or crush

94
Q

what is specific about taking a nystatin suspension

A

you must swish for a few minutes and swallow

after you’ve given nystatin, the patient should not eat or drink anything for 20 minutes.

95
Q

when using a powder what do you need to ensure to make sure the medication works

A

the skin you are applying the powder to, you need to make sure the area is clean and DRY

96
Q

what are adverse effects of nystatin

A

oral form:
cramps
topical:
skin irritation

97
Q

how can a fungal infection be systemic

A

from the inhalation of spores which will affect the respiratory system and their lungs

98
Q

where is histoplasmosis found and how transmitted

A

found in bird and bat droppings

transmitted via airborne

99
Q

when will you see symptoms of histoplasmosis

A

3-17 days after exposure to the spores

100
Q

what is aspergillosis

A

a type of mold that can be a problem in pts with immunocompromised systems.

101
Q

where is aspergillosis aquired

A

either in the hospital or environment sources.
either decaying leaves of plants, trees, shrubs
or inside such as A/C or ventilation ducts.

102
Q

who does aspergillosis affect

A

people with weakened immune systems

healthier people usually do not have a problem

103
Q

what causes valley fever

A

coccidioides

104
Q

what does cocciodiomycosis affect

A

infects the lungs and can become disseminated

105
Q

where can you find cocciodiomycosis

A

in the soil in the US and parts of mexico

106
Q

s/s of systemic fungal infections

A 
dry cough
wheezing
SOB
fever
chest pain
fatigue
body aches
107
Q

when may you see symptoms of coccidiomycosis

A

between 1-3 weeks after the pt inhales the spores.

108
Q

what can fluconazole be used for

A

oropharyngeal or esophageal candidiasis or systemic infections

109
Q

what medication can be taken for thrush

A

fluconazole

110
Q

how does fluconazole work

A

inhibits fungal steriles- disrupts the cell membrane of the fungus allowing the contents of the fungal cell to leak out

111
Q

how is fluconazole excreted

A

10% metabolized by liver

80% unchanged by the kidneys

112
Q

side effects of fluconazole

A

crystalluria- drug can crystallize in tubules
GI distress
S-J syndrome with immunosupporession

113
Q

what should you monitor while on fluconazole

A

LFTs
BUN Creatinine
urine
adequate hydration

114
Q

what drug interactions does fluconazole have

A

warfarin
-may increase risk of bleeding with warfarin
glipizide and glyburide
-increasing hypoglycemic effects

115
Q

what is amphotericin B used for

A

treatment of progressive, potentially fatal systemic fungal infections
systemic candida, histoplasmosis, aspergillosis and cocciodiomycosis
-pts who have tried fluconazole without help or the fungal infection is so severe they need something more.

116
Q

how does amphtericin B work

A

binds to fungal cell wall disrupting cell membrane
in healthy ppl a lower dose may be given to kick start a fungistatic effect helping the host cell to take over
in higher doses it becomes fungicidal

117
Q

what is the strongest antifungal med

A

amphotericin B

118
Q

what is the problem with amphtericin B

A

it has a risk of acute infusion reactions and nephrotoxicity

119
Q

how long can amphotericin B be detected

A

up to 7 weeks

120
Q

what are adverse effects of amphotericin B

A 
N&V
Diarrhea
nephrotoxicity
chest pain
hypotension, elevated liver enzymes, 
hypokalemia, 
chills
fever,
phlebitis
121
Q

what do nurses do to reduce the chances of side effects of amphotericin B

A
  • Vital signs q1h (watch for hypotension, fever)
  • assess anaphylaxis (severe allergic reaction)
  • adequate hydration 2-3L fluid/day (reduce kidney damage)
  • pre medicate with anti-emetics and antipyretics, antihistamines, corticosteroids, analgesics (d/t the such high risk of adverse effects)
  • monitor infusion closely(continue asking how they are doing)
  • infuse slowly- over 2-6 hrs
122
Q

what does metronidazole treat

A 
Broad spectrum
it is a bactericidal
trichomonacidal
amebicidal
capable of killing parasites
123
Q

how does metronidazole work

A

disrupts DNA and protein synthesis

124
Q

patients who have what would receive metronidazole

A

patients with anaerobic type infections such as intra abdominal infections

  • skin-skin structures
  • lower respiratory tract infections
  • septicemia
  • bone/joint infections
  • mild to moderate c-diff (without any other complications)
125
Q

forms of metronidazole

A

oral and IV forms

126
Q

if a pt has c-diff which form of metronidazole would you give

A

oral form

because you need the med to go through the GI tract

127
Q

what is special about the IV form of metronidazole

A

the IV form is also effective in treating C-diff, the ONLY one

128
Q

what does metronidazole PO cover

A

dysentery (inflammation/ulceration of lower part of bowel- pts suffer from bloody diarrhea)
Trichomoniasis- STI caused by parasite
peptic ulcer disease- caused by H Pylori

129
Q

what are the adverse effects of metronidazole

A 
abdominal pain
anorexia
dizzy
dry mouth
 metallic taste
130
Q

what drug interactions does metronidazole have

A

warfarin

it increases the effects of warfarin

131
Q

What is diabetes the leading cause of

A

Blindness
Renal failure
Non traumatic leg amputations

132
Q

What is diabetes characterized by

A

High glucose levels and the body’s inability to use or produce insulin

133
Q

What are major risk factors for diabetes

A

Obesity and sedentary lifestyle

134
Q

Is diabetes cureable

A

If it is caught in the ore diabetic stages. Yes it can be reversed by lifestyle and diet modifications.
If the pt is diagnosed with diabetes then no it is not cureable. It at that point has to be treated and managed.

135
Q

What is diabetes.

A

A CHO metabolism disorder

A multi factoral multi organ condition

136
Q

What can diabetes predispose patients to

A

Cardiovascular disease
Renal damage
PVD
Eyes and nervous system disorders

137
Q

What are immediate complications of hyperglycemia

A
  • WBC cells do not work effectively. (The T cells and phagocytic effect is deminished causes the immune system to be less effective causing immunosuppression)
  • Which leads to poor wound healing
  • Increases colonization of staph aureus (these pts already have an increase in susceptibility-which affects wound healing)
  • Frequent occurrence of UTI, yeast infections, and soft tissue infections

-Increase in coaguability of RBC

138
Q

What does chronic hyperglycemia do to the arteries of the body

A

It causes angiopathy because the endiothelial lining is injured which causes the arterioles to narrow(arteriosclerosis) the narrowing can lead to HTN

139
Q

What are the hyperglycemic complications related to microvascular angiopathy

A

Retinopathy- the smallest arteries in our retina are damaged
Neuropathy-damage to sensory and motor neurons
Nephropathy- damage to arterioles around the nephron

140
Q

What causes diabetic retinopathy

A

The hyperglycemia caused endothelial injury in the retinal arterio vessels which cause inflammation and cause platelets to respond clogging the arteries and capillaries leading to retinal ischemia

141
Q

What can retinopathy lead to

A

If not treated it can lead to seeing spots
Unclear vision
Eventually blindness

142
Q

What causes diabetic neuropathy

A

Hyperglycemia damages the arterioles that supply nutrients to the neurons and the neurons begin to demyelinate and degenerate in the nerve fibers of the lower extremities first

143
Q

What are symptoms of neuropathy

A

Numbers
Tingling
Pain
Sensitive to touch

Causing weakness and unsteady gait

144
Q

What can nephropathy lead to

A

Renal insufficiency and renal failure due to the damage to the arterioles around the nephron

145
Q

What does hyperglycemia do to the glomerular capillaries

A

Damages them causing them to become hyperpermeable causing proteins and other substances leak out
Leading to proteinuria and microalbuminuria

146
Q

What are the complications of hyperglycemia related to macrovascular angiopathy

A

Coronary artery disease
Cerebrovascular disease
PVD

2-4x at risk of a cardiovascular event

147
Q

How does hyperglycemia affect the macrovascular arteries

A

It damages them causing arteriosclerosis leading to -HTN leading to myocardial ischemia

  • TIA-decreased blood flow to the brain
  • PVD
148
Q

Which islets of langerhans cells produce insulin

A

Beta cells

149
Q

What stimulates beta cells to release insulin

A

The rise in blood glucose

150
Q

What is insulin

A

An anabolic hormone that has body building function

It can build muscle, store fat and form glycogen

151
Q

Where is excess glucose stores

A

In the liver and muscles in the form of glycogen
Or
In adipose tissue as fatty acids

152
Q

What areas of the body do not need insulin

A

The brain and the contractile muscle

153
Q

What do alpha cells produce

A

Glucagon which is an opposing hormone to insulin

It is secreted when blood sugar is LOW

154
Q

What does glucagon do

A

1-glycogenolysis: breakdown of glycogen to glucose

2-activate gluconeogenesis: making new glucose from amino acids and lipids. (Gluconeogenesis has the ability to activate lipase which breaks down fat)

155
Q

What happens when fat breaks down

A

It is broken down into fatty acids and glycerol

The glycerol is what is used to make glucose

The fatty acids break down to keytones which can lead to diabetic ketoacidosis

156
Q

Type 1 diabetes vs type 2

A

-type 1
Occurs more in adolescent.
Caused from predisposition,genetic factor, autoimmune response
End result-lack of insulin production
-type 2
Either causes from not enough insulin or insulin resistance
Caused from obesity and sedentary lifestyle
End result need oral or insulin therapy

157
Q

what is insulin resistance characterized by

A

cellular resistance to insulin which causes the pancreas to work even harder, leading to hyperinsulism
this leads to an overworked and exhausted pancreas leading to a decrease in insulin production

158
Q

what happens after the pancreas becomes weak and tired and begins to produce less insulin

A

the blood glucose rises and stays higher

159
Q

what are the two contributing factors to insulin resistance

A
  1. the lack of physical activiyt

2. obesity

160
Q

why is obesity a contributing factor to insulin resistance

A

because fat cells are more resistant to insulin

161
Q

how does physical activity help with diabetes

A

physical activity can improve our cells sensitivity to insulin and improve glucose uptake

162
Q

what is a condition of type 1 diabetes

A

Diabetic Ketoacidosis
because there is not enough insulin so the alpha cells perform gluconeogenesis which results in the breakdown of fat causing increase of keynotes leading to DKA

163
Q

walk through the steps of hypoglycemia development

A
  • glucose absorbed via GI
  • glucose stimulates pancreas to secrete insulin
  • body cells resist insulin/glucose can’t enter cells
  • glucose accumulates in the bloodstream
  • pancreas continues to put out insulin
  • cells may be resistant to insulin causing hyperinsulinemia
  • cells feeling starved-
  • -liver will break down glycogen to glucose and break down fats and amino acids to further increase glucose
164
Q

what are risk factors for developing diabetes that cannot be controlled

A 
age (older)
family hx- especially a 1st degree relative
hx of gestational diabetes
ethnicity 
genetic mutations
165
Q

what ethnicities are at greater risk for diabetes

A

african-american
asian-american
hispanic
native american

166
Q

what are risk factors for diabetes that can be controlled

A
  • obesity/diet
  • lack of physical inactivity
  • metabolic syndrome
167
Q

what is metabolic syndrome and what has to be present to qualify

A

group of risk factors that raises the risk for developing heart disease, diabetes, stroke, coronary artery disease, PVD, thromboembolic events

have to have 3 of 5:

  • hyperglycemia
  • abdominal obesity (apple shape)
  • decreased HDL
  • high BP
  • high triglycerides
168
Q

when should you perform a fasting blood glucose test

A

after 8 hours of NPO

169
Q

What is OGTT

A

oral glucose tolerance test

pt will ingest 75g CHO drink and 2 hours later the glucose will be assessed.
this is to assess how the pancreas is working

170
Q

what can blood glucose diagnostics tell us

A

it will tell us if the pt has hyperglycemia, diagnose pre or diabetes, and can also be used to tell how people are controlling their hyperglycemia

171
Q

How does the hgb A1c work

A

it is used to assess the blood glucose control over 120 days..
glucose attaches irrevirsibly to hgb molecules and survives for the life of the RBC.
the A1c does not show peaks or valleys but gives us an understanding of how hyperglycemia has been. indicates how therapy has been or to diagnose diabetes.

172
Q

what levels of fasting blood glucose is diabetic

A

normal: <99
pre diabetic: 100-125 on TWO separate occasions
diabetic >126 - on TWO separate occasions

173
Q

what are the levels of hgbA1c

A

normal: 5.6
pre diabetic: 5.7-6.5
Diabetes: >6.5

174
Q

what are the levels of 2 hr post OGTT

A

normal: <139
pre diabetic: 140-199
diabetes: >200

175
Q

level to diagnose diabetes with a random blood glucose test

A

> 200 with symptoms

176
Q

what are ways to modify lifestyle for pre diabetest/diabetes

A
  • follow a meal plan that has a balanced CHO intake w/ pancreas function
  • increase intake of healthy foods.
  • low sugar, low CHO
  • increase activity level-promote weight loss and muscle growth (exercise can reduce insulin resistance)
  • self monitor glucose levels
177
Q

what is encouraged in a diabetic diet

A

Protein
it can slow down digestion and slows the rise of glucose
high protein can stimulate insulin response but does not cause insulin spikes
should have intake of 15-20%/day

178
Q

what effect does fat have on blood glucose

A
  • slows digestion which slows the rise of glucose
  • promotes the feeling full (eats less)
  • should have less than 7% saturated fats.
  • intake should be 25-30% calories/day
179
Q

what effect does alcohol have on blood glucose

A

-inhibits gluconeogenesis therefore can cause hypoglycemia in pts taking insulin (because new glucose cannot be formed)
recommendation:
-drink in moderation- women 1/day, men 2/day
-drink w/ meals, sugar free mixes, dry or white

180
Q

CHO effects on glucose and recommendations

A

-contribute to post prandial glucose spikes.
-include sugars, starches and fibers
promote healthier CHO such as whole grain bread, fruits and veggies.
daily allowance 130g/day
50% of calories/day

181
Q

how many grams is 1 serving of CHO

A

1 serving CHO = 15 grams

182
Q

what is the recomendation for patient who are on antiglycemic agents

A

that they do not skip meals and have snacks throughout the day

183
Q

how many grams of CHO should a person have each meal

A

45-60 grams/meal
and 15-30grams/snack
130 is the minimum

184
Q

how is my plate separated

A

1/2 plate veggies, 1/4 starch, 1/4 protein and a side of dairy and fresh fruit

185
Q

what is the first line drug choice for type 2 diabetes or preventing type two

A

metformin
(abiguanide)
either a mono therapy or a used with other oral or insulin meds

186
Q

how do biguanides work

A
  • they make body tissues less resistant to endogenous insulin (more sensitive to the insulin our body makes)
  • decrease the amount of glucose produced by the liver
  • decrease the intestinal absorption of glucose
187
Q

what are the adverse effects of metformin

A

nausea
diarrhea
abdominal bloating (can cause ppl to not eat as much because they feel full so may cause weight loss)
metallic taste

188
Q

what are nsg implications of metformin

A

-med needs to be taken with meals

189
Q

what is metformin contraindicated in

A

-renal insufficiency

because it is almost completely eliminated in the kidneys

190
Q

how long should metformin be held if a pt is going for a test with radiographic contrast

A

needs to be held at 1-2 hours BEFORE the procedure and 48 hours AFTER procedure

191
Q

what should you do before starting metformin after a pt has gone for a test with contrast

A
  • need to check kidney function BUN/Creatinine

- need an order to restart med.

192
Q

what are the 3 sulfonylureas

A

glipizide
glyburide
glimepiride

193
Q

what are the actions of sulfonylureas

A
  • lower blood sugar by stimulate release of insulin
  • increase sensitivity to insulin at receptor sites
  • decrease hepatic glucose production
194
Q

what are adverse effects of sulfonylureas

A 
hypoglycemia
increased appetite (d/t the increased insulin)- may cause weight gain
195
Q

s/s of hypoglycemia

A 
sweating 
hunger
weakness
dizziness
tremors
tachycardia
anxiety
196
Q

what are nursing implications when administering sulfonylureas

A
  • administer meds 30 min BEFORE meals
  • assess for sulfonamide allergies
  • assess liver function because these meds are metabolized by the liver.
  • hold during post op until pt is intaking regular meals to prevent hypoglycemia
197
Q

which med can sulfonylureas be given concurrently with to help therapy

A

metformin

198
Q

what are incretins

A

natural stimulating hormones that are found in the GI tract.
in response to food they stimulate pancreatic insulin secretion

199
Q

what would incretin dysfunction result in

A

post parandial hyperglycemia
because the incretin is not working correctly and not detecting food therefore cannot stimulate the pancreas to secrete insulin

200
Q

what is DPP 4

A

di peptidyl peptidase 4
an enzyme that destroys incretin hormones.
found in obese pts and pts with insulin resistant type diabetes

201
Q

what do DPP 4 inhibitors do

A

a medication that inhibits the DDP 4 enzyme from destroying the incretins thus allowing the incretins to stimulate the pancreas to secrete insulin and reduce fasting BG and post parandial BG

202
Q

what are DPP 4 inhibitors used for

A

the management of type 2 diabetes

203
Q

what are the DPP 4 inhibitor drugs

A

Sitagliptin (januvia)

Saxaglipitin

204
Q

what is the combo DPP4 inhibitor drug

A

sitagliptin and metformin (JANUMET)

205
Q

what drug interactions are with DPP 4 inhibitors

A

increased risk for hypoglycemia with sulfonylureas or insulin

206
Q

what are the nursing implications for DPP 4 inhibitors

A

-administered w/o regards to food
-sx pts may need to be stopped pre op/post op-check w/ md
-check glucose levels
assess for s/s of hypoglycemia
-sweating
-hunger
-weakness
-dizziness
-tremors
-tachycardia
-anxiety

207
Q

what is the goal of insulin therapy

A

to mimic the pancreatic pattern of pancreatic secretions of insulin without causing hypoglycemia

208
Q

what are they types of insulin

A

rapid
short
intermediate
long acting

209
Q

what are the rapid acting insulins and when are they given

rapid acting do not LAG

A

lispro
aspart
glulisine
(lispro and aspart are the same and interchangeable)
they are given 15 minutes before a meal. given 3-4 times/day

210
Q

what are the short acting insulins

and when are they given

A

Humilin R
Novolin R
they are given 30-60 minutes before a meal

211
Q

what are the intermediate acting insulins and what is special about them

A 
humulin N
Novolin N
a suspension 
it is the only insulin that looks cloudy
it is given twice a day 
it can be mixed with short or rapid acting insulin
212
Q

what are the long acting insulins and what is it used for

A

Glargine
Detemir
(no peak and last 24+hrs)
-its used to control the fasting plasma glucose level.
-released steadily and continuously and mimics pancreas delivery of insulin
-given once daily

213
Q

what is a basal bolus insulin regimen

A

a one daily injection of long acting insulin with several short acting insulin blouses
approximates normal patterns
requires frequent glucose monitoring AC and HS

214
Q

what are other factors that can affect glucose levels

A
  • corticosteroids

- stress

215
Q

how does corticosteroids and stress cause hyperglycemia

A

increase glucose levels

  • corticosteroids promote glucose production from the liver and reduce cell sensitivity to insulin
  • stress can increase glucose levels

202D (6 decks)

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