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202D > Test #3 > Flashcards

Test #3 Flashcards

1
Q

after how long of not having adequate oral intake will the Dr consider TPN

A

about 7 days

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2
Q

what are some indications for TPN

A
  • chronic severe diarrhea and vomiting
  • complicated surgery or trauma
  • gi tract anomalies
  • severe malabsorption
  • GI obstruction
  • severe anorexia
  • short bowel syndrome
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3
Q

what is short bowel syndrome and why is TPN considered for this condition

A

part of small intestine is removed or missing.
in our small intestine is where a lot of our absorption takes place.
therefore w/ short bowel syndrome you don’t have the surface area to absorb the required nutrients

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4
Q

what is PPN

A

partial or peripheral parenteral nutrition

  • usually administered via peripheral line
  • it doesn’t meet energy and caloric requirements long term.
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5
Q

what is the osmolarity of PPN and why is it not any higher?

A

900mOsm/ L

the higher the osmolarity the higher risk for phlebitis

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6
Q

what does PPN do

A

support inadequate oral intake to help the body meet caloric requirements

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7
Q

can the pt take in food orally if they have PPN

A

yes.

PPN can be used with or without added oral intake

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8
Q

How long should someone be on PPN

A

a person should not be on PPN for more than 2 weeks.

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9
Q

how often is PPN administered

A

It can be around the clock or in cycles

  • in the hospital it is usually on a continuous cycle.
  • if pt is going home on PPN it can be in cycles especially if they are eating orally
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10
Q

what does PPN require in order to protect the vitamins

A

the bags need to be covered with a brown bag to block out the light because light can inactivate the vitamins in the solution.

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11
Q

what is the osmolarity for TPN and where is it administered

A

1500-2800mOsm/L

and it is administered via central line

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12
Q

why is TPN given

A
  • to correct nutritional deficits

- for patients who require long term nutritional replacement to meet energy and caloric requirements.

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13
Q

why are TPN bags smaller than PPN bags

A

because of the higher osmolarity of the TPN

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14
Q

what do you assess for with a pt on PPN or TPN

A
  • monitor electrolyte levels!
  • monitor blood pressure trends
  • assess weight daily
  • listen to lung sounds to monitor for fluid overload
  • Monitor kidney function-to make sure they can tolerate the excess volume
  • monitor liver function- pts with liver failure may have a lower protein intake so adjustments need to be made
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15
Q

why assess protein level prior to start of TPN

A

because the pharmacist needs to adjust the amino acids in the bag.

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16
Q

what 2 labs are used to assess how severely malnourished the pt is

A

pre albumin and albumin

protiens made by the liver used to assess nutritional status

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17
Q

what is the range for pre albumin and half life

A

17-40mg/dL

half life:2days

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18
Q

what does the body use pre albumin for

A
  • protein synthesis

- bind and transport proteins in the body

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19
Q

why do we look at pre albumin

A

to determine if the patient is getting enough protein and to figure out what the patients malnutrition risk is or if they already are malnourished
and to monitor parenteral nutrition and to assess if it is effective

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20
Q

what lab value is sensitive to change in our protein energy status

A

pre albumin

it more closely resembles what the protein dietary intake is.

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21
Q

what level of pre albumin would indicate the patient is severely malnourished

A

a pre albumin level of <10mg/dL

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22
Q

if a patients pre albumin level is <5mg/dL what will that indicate

A

severe protein depletion

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23
Q

what is albumin range and half life

A

3.5-5.0g/dL

half life 20-24 days

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24
Q

what do we need albumin

A
  • protein type that we need to maintain growth and repair tissues.
  • it also carries nutrients and hormones
  • maintains intravascular pressure
  • inhibits ascites from forming
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25
Q

what does albumin tell us

A

whether a patient has been chronically malnourished or not.

it cannot tell us if the pt is acutely malnourished

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26
Q

what will happen if a patient is deficient in albumin and is started on peripteral nutrition

A

the pt will develop edema because the decreased albumin causes a decrease in colloidal pressure thus allowing fluid to move out of the vessels.

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27
Q

what does a decreased albumin level indicate

A
  • severe malnutrition

- liver and kidney disease

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28
Q

what does an increased albumin level indicate

A

dehydration
vomitting
diarrhea
(caused from concentration d/t volume loss)

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29
Q

what are the macro nutrients in PN

A

-water=base
-dextrose
-amino acids
-lipids- (in separate bag but infused with TPN)
plus added electrolytes vitamins trace elements

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30
Q

who is in charge of monitoring pts electrolyes

A

the pharmacist because the have to adjust the therapy
but
YOU need to assess their levels as well and you need to call them with any abnormal levels

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31
Q

what is the primary source of calories in PN

A

dextrose

it provides up to 70-85% of caloric intake

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32
Q

what is something you need to monitor in relation to the dextrose in PN

A

BLOOD GLUCOSE
you need to assess pts glucose response
(dextrose is gradually increased or decreased depending on pts response)

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33
Q

when checking blood glucose for pt on TPN how often are you checking the blood sugars

A

usually the orders will call for Q6H and then qPM

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34
Q

why are amino acids needed in TPN

A

because they are needed to synthesize more proteins
help conserve muscle mass
help wound healing
1 gram amino acid = 1gram protein

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35
Q

what would cause the need for a decrease in protein requirement for TPN

A

hepatic or renal disease

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36
Q

why is protein important when we have a lot of CHO intake

A
  • it slows digestion

- it blunts the hyperglycemic response

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37
Q

what are lipids for in TPN and why the body needs them

A

a dense source of calories

  • blunts the hyperglycemic response
  • need to form healthy cell membranes
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38
Q

what is the main fat source in the lipid bag

A

soy bean oil or

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39
Q

what do some electrolytes contain

A

acetate salts which are converted by the liver to bicarbonate allowing the body to maintain acid base balance.

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40
Q

what do you need to do if the pt is iron deficient and needs iron

A

they can either take PO iron
or
they can have IV infused separately
iron is not compatible with parenteral nutrition
(can be same site as long as it is compatible with the infusing bag)

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41
Q

what are hyperglycemia symptoms

A
  • extreme thirst
  • polyuria
  • dry skin
  • polyphagia
  • blurry vision
  • drowsy
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42
Q

what can be added as well when a person is on PN

A

if the person has problems controlling their blood glucose so therefore the pharmacist can add insulin to the bags to help control the glucose

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43
Q

what may need to be ordered in addition to parenteral nutrition therapy

A

-glucoscans
AND
-sliding insulin scale to help the body maintain glucose levels if the pt is not tolerating the therapy well.

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44
Q

what is the glucose goal for a patient on PN therapy

A

<200mg/dL- at the initiation of therapy

throughout therapy we want glucose to be around 110-150

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45
Q

what is rebound hypoglycemia

A

a possible complication of PN

  • while getting higher levels of dextrose the body secretes a larger amount of insulin to compensate leading to hyperinsulinemia
  • this condition can result when he infusion is stopped abruptly- therefore there is an abrupt drop in glucose and an abundance of insulin causing hypoglycemia
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46
Q

what do you need to do when stopping parenteral nutrition therapy

A

gradually decrease to prevent rebound hypoglycemia

- you need to decrease the rate by half and run at that rate for an hour and then you can turn it off

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47
Q

what do you do if the PN bag is empty when you check on your pt

A

-call the pharmacy
-hang D10W or D20W running at the same rate as the PN
because you need to prevent rebound hypoglycemia
- you do not need an order to hang d10 or d20 in this situation because the PN order covers this because you don’t want PN therapy to abruptly stop

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48
Q

S/S of hypoglycemia

A 
shaky
lethargic
head ache
blurry vision
cold/clammy
tachy
sweaty
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49
Q

what are complications of parenteral nutritional therapy

A
  • hyperglycemia
  • rebound hypoglycemia
  • refeeding syndrome
  • fluid overload
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50
Q

How does refeeding syndrome occur

A

when we supply a severely malnourished or chronically starved pt parenteral nutrition
(these pts have gone through glycolysis and have started gluconeogenesis so their main source of energy is protein and fats)
when we reseed with PN and use dextrose as 30% of caloric intake this stimulates increase in insulin which pulls glucose into cells but insulin also pulls K+, Mg and phosphate into cells as well.
-so the already depleted electrolyte levels in the blood become even more depleted

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51
Q

what are the hallmark conditions of referring syndrome

A

hypophosphatemia
hypokalemia
hypomagnasemia

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52
Q

s/s of refeeding syndrome

A

mostly related to hypophosphatemia

  • cardiac dysrhythmias
  • repsiratory arrest
  • neurological disturbances
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53
Q

what is HTN a risk factor for

A 
CAD
CVD
HF
renal failure
PVD
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54
Q

what are the non modifiable risk factors for developing HTN

A

-family history-30-40%
-Age- vessels lose elasticity with age-
-Gender-
more common in males up to the age of
45
more common in women after the age of
65 (d/t onset of menopause)
equal occurrence in men and women 45-64
-Ethnicity-
african americans are more sensitive to salts causing them to be more at risk for HTN
Hispanics at greater risk b/c they are less likely to receive tx and management is lower and lower level of awareness

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55
Q

for african americans how much salt will cause an increase in BP

A

1/2 teaspoon of salt can raise BP 5mmHg

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56
Q

how do African Americans control their BP

A

have a low sodium diet and usually need more than one drug to help lower BP

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57
Q

what are the modifiable risk factors for HTN

A
  • lack of physical activity- this leads to being over weight and being overweight puts more strain on the heart.
  • 11-20lb weight gain can cause a measurable amount of increased BP
  • Diet- high calorie, fat, sugar-increases obesity…high salt attracts more water leading to more strain on the heart (especially for african americans)
  • Alcohol-
  • smoking & second hand- increase risk of artery damage
  • Stress-
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58
Q 
stages of hypertension 
normal
pre hypertensive
hypertensive stage 1
hypertensive stage 2
hypertensive crisis
A

staged on the average of 2 or more properly measured BP readings on 2 or more office visits
-Normal– SBP <120 AND DBP <80

  • Pre hypertensive- SBP 120-139 OR DBP 80-89 (lifestyle modifications need to start
  • HTN stage 1–SBP 140-159 OR DBP 90-99
  • HTN stage 2–SBP 160 or higher OR DBP 100 or higher
  • HTN crisis–higher than SBP 180 OR DBP higher than 110
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59
Q

for a pt over the age of 60 w/ no diabetes or ckd what is their BP goal

A

SBP <150

DBP <90

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60
Q

for pts with no CKD or diabetes present what would be the rx treatment

A 
for non black pts:
initiate thiazide diuretics
Ace inhibitors
ARBs 
calcium channel blockers

For black pts
initiate thiazide diuretics
calcium channel blockers

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61
Q

for pts with diabetes but no ckd what would the rx treatment be

A 
for non black pts.
initiate thiazide diuretics
Ace inhibitors 
ARBs
calcium channel blockers

For black pts
initiate thiazide diuretics
calcium channel blockers

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62
Q

for pts with CKD and with or without diabetes what is the Rx treatment

A

for all races
initiate ACE inhibitors or ARBs
alone or in combo with other drug classes

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63
Q

what are contributing factors for primary HTN

A
  • increases SNS activity
  • increased Na+ intake
  • over production of aldosterone
  • increased BMI
  • Diabetes
  • Smoking
  • chronic/ excess use of alcohol
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64
Q

what is 2ndary HTN

A

HTN from an underlying cause that can be identified and corrected

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65
Q

how does HTN affect the vessels

A

-can lead to angiopathy(arteries and arterioles)-
the vessels thicken as a protective measure against the increased pressure but over time the thickening causes narrowing of the vessel and also decreases in flexibility

-HTN plays a role in atherosclerosis- plaque formation which causes narrow, less flexible vessels

66
Q

how does HTN affect the heart

A

-d/t the antipathy and the atherosclerosis formation caused from HTN
blood can flow through the heart very well leading to coronary artery disease, chest pain and MIs

67
Q

how does HTN affect the brain

A

plaques can form in the common carotid artery inhibiting blood flow leading to a stroke and TIAs
ppl who have TIAs are more at risk for having full stroke

68
Q

how does HTN cause PVD. what happens

A

HTN can lead to atherosclerosis which leads to PVD- intermittent claudication
leg pain caused by ischemia
excess activity increases the blood flow but because of the plaque formation blood cannot flow easily through the lower extremities resulting in pain

69
Q

How does HTN affect the kidneys

A

it causes nephrosclerosis
there are a lot of arteries that supply our kidneys so when those arteries become atherosclerotic our kidneys will decline in function and are unable to filter as well.
nephrons begin to die and kidney function decreases.
renal disease can develop from ischemia from the arteries supplying kidneys becoming atherosclerotic
those nephrons will eventually atrophy and die affecting the glomerulus.

70
Q

how does HTN affect the retina

A

the vessels in the eye become atherosclerotic causing small hemorrhages leading to blurred vision or vision loss.
pts with severe retinal damage may see spots

71
Q

what is the short term mechanism for bp

A

the ANS is stimulated and the Baroreceptors are activated when they sense low BP
the transmit a signal to the brain stem that will cause an increase in cardiac contractility, increase HR and increase vasoconstriction causing an increase in BP

When baroreceptors sense an elevated BP they send inhibitory signals to the brainstem
causing a decrease in HR, decreased contractility and vasodilation

over time if BP is not managed the baroreceptors become accustomed to the higher blood pressure and accept it as normal

72
Q

Explain the RAAS system

A

The liver synthesizes and releases angiotensinogen
the kidneys release renin (in response to decreased bp, low volume, low Na, high urine na+)

  • RENIN converts angiotensinogen to angiotensin I
  • angiotensin I circulates until it comes in contact with angiotensin converting enzyme (secreted by endothelial cells of LUNGS)

-ACE converts angiotensin I to angiotensin II

-Angiotensin II stimulates vasoconstriction=increased BP
also stimulates adrenal cortex to stimulate the release of aldosterone

  • aldosterone increases reabsorption of Na+ and H2O in distal tubule = increased ECF volume and increasing BP
    • (when Na+ and H2O reabsorbed K+ is lost)
73
Q

what happens when there is a long term presence of angiotensin II

A

-can cause cardiac remodeling=
enlargement of heart cells.
collagen deposits that form scar like tissue in the heart.

leading to Heart Failure b/c an enlarged heart with scar tissue cannot maintain the normal cardiac output

also causes release of chemical mediators of atherosclerosis
-deposits fatty plaques in vessels and heart that leads to MI and Strokes

74
Q

How to identify name of ACE inhibitors

A

they have “pril” at the ending

75
Q

what is a first line drug for HTN

A

ace inhibitors

76
Q

what is the job of an ace inhibitor

A

to inhibit conversion of angiotensin I to angiotensin II

-reduces systemic vascular resistance and decreasing aldosterone secretion

77
Q

what is a benefit of ace inhibitors

A

because of what ace inhibitors do, they help the heart.
it can stop the progressive cardiac remodeling of the heart.

so this is why ace inhibitors are cardioprotective-they benefit in the tx of heart failure

the protect the renal system because they cause efferent arteriole to vasodilate which can decrease glomerular filtration pressure.

78
Q

common side effects of ace inhibitors

A
  • dry cough
  • ED
  • orthostatic hypotension
  • possible hyperkalemia-d/t the excretion of Na+ and h2o b/c the inhibition of aldosterone
79
Q

who would be more at risk for hyperkalemia when taking ace inhibitors

A

ace inhibitors are 100% metabolized and excreted by kidneys-

pts with CKD
using spironolactone (K+ sparing diuretics)
K+ supplements

80
Q

what are ARBs

A

angiotensin II receptor blockers
-ends in “TAN”

block angiotensin II
in the arterial smooth muscle and in adrenal gland thus blocking the secretion of aldosterone
also receptors in the heart- preventing cardiac remodeling

81
Q

which med is best used for heart failure

A

Ace inhibitors because the ace inhibitors block the formation of angiotensin to and with ARBs the angiotensin II is already formed

82
Q

what else is losartan used for

A

diabetic nephropathy

83
Q

what are adverse effects of Losartan

A
  • Hypotension
  • Hyperkalemia
  • hypoglycemia
84
Q

would losartan and lisinopril be used together

A

NO because they have a similar action

85
Q

what are alpha 1 blockers

A

Doxazosin and tamsulosin
the alpha 1 receptors are in the arteriole and venous smooth muscle (these vessels feed the heart, renal and GI system)

activation of these receptors causes constriction therefore blocking the receptors causes vasodilation =decreased resistance = decreased BP

when we block the receptors -b/c we have them in our bladder- it will relax the muscle in the bladder which is why tamsulosin is used for BPH

86
Q

what are adverse effects of alpha 1 blockers

A

dizziness
head ache
decreased libido/sexual dysfunction
orthostatic hypotension (when first dose given within 24 hrs)

87
Q

when should a person take an alpha 1 blocker

A

at bedtime to reduce the risk of orthostatic hypotension and falling causing further injury

88
Q

what are alpha 2 agonists

A

clonidine

  • acts in the CNS to decrease sympathetic activity
  • the activation of alpha 2 receptors causes vasodilation

-helps control BP by stimulating alpha 2 receptors in the PRE synapse to accept more norepinephrine that way less nor epinephrine in the synaptic cleft. (keep more norepinephrine in the pre synapse)
{norepinephrine causes vasoconstriction}

89
Q

what are side effects of alpha 2 receptors

A

dry mouth
drowsiness
withrdawal phenomenon-caused from an abrupt stop of taking medication that can lead to rebound HTN and increase HR

90
Q

what should a pt do if they are stopping clonidine

A

they need to titrate down to prevent withdrawal phenomenon

91
Q

who should receive clonidine

A

pts who are very HTN resistant. Pts who are on other hypertensives and still have HTN

not a first line drug

92
Q

what is the vasodilator drug

what are they used for and in conjunction with?

A

Hydralazine (most common)
not first line
used for moderate to severe HTN
usually in conjunction with diuretic

93
Q

what does hydralazine do

A

help dilate blood vessel
and relax arterial smooth muscle to reduce vascular resistance
prevent arterial walls from tightening and narrowing
helps increase blood flow and help heart not pump as hard

94
Q

what is a possible adverse reaction of hydralazine

A

has a higher probability of hypotensive effect which can cause the body to sense a low perfusion causing the heart to increase cardiac output resulting in tachycardia

other possibilities
edema and orthostatic hypotension

95
Q

what is DASH

A

dietary approaches to stop HTN
emphasizes decrease in take of salt and sugar
increase more fruits, vegetables,
decreased red meats, fat free or low fat dairy
increase whole grains,
increase chicken
increase beans seeds nuts fiber

96
Q

what should the Na+ intake be

A

a normal healthy adult = < or = 2300mg/day to maintain normotension
African Americans, HTN, diabetics, CKD= < or =1500mg/day

97
Q

what are some lifestyle modifications for maintaining healthy bp

A

-lose weight- BMI brown 18.5-24.9
(also helps improve glucose uptake)
-increase physical activity (30min) 4x/wk
-decrease alcohol use
-no tobacco-nicotine causes -vasoconstriction- increases BP and risk for CVD
-learning how to deal with stress in a healthy way
-compliance with drug therapy

98
Q

what is asthma

A

inflammation, swelling and mucus production

bronchospasm

99
Q

what triggers asthma

A
  • allergens
  • air pollutants
  • respiratory infections
  • Gerd
  • exercise
  • drug therapy
100
Q

what are s/s of asthma

A 
SOB
wheezing,
cough
chest tightness
prolonged expiration
hyperinflation of alveoli (air is trapped in alveoli)
101
Q

what is the treatment for asthma

A

selective beta 2 adrenergics

102
Q

what are the short acting beta 2 agonist

A

albuterol

-used to relieve acute symptoms

103
Q

how does albuterol work

A

it selectively binds to beta 2 receptors which facilitate bronchial dilation,
mucous drainage
inhibiting release of inflammatory chemicals such as histamine and interleukins

104
Q

what is the onset and duration of action for albuterol

A

onset- 5-15minutes
duration 2-6 hours
why it is a rescue medication

105
Q

side effects of albuterol

A

nervousness
shaky
tremors
palpitation

106
Q

what is a long acting beta 2 adrenergic

A

salmeterol diskus

107
Q

what is salmeterol diskus used for

A

long term prophylaxis and long term therapy for COPD

108
Q

what is the duration of action for salmeterol diskus

A

up to 12 hours with a slow onset

109
Q

what is a side effect of salmeterol diskus

A

headache

110
Q

what are leukotrienes

A

a substance that is released during an asthma attack
they are primarily responsible for bronchiole constriction
mucus production and edema

111
Q

what is the leukotriene receptor antagonist

A

Montelukast

non steroidal

112
Q

what does montelukast do

A

binds to leukotriene receptors in respiratory tract and blocks them

this vasodilates the bronchioles
decreases mucous secretions and
improve edema

113
Q

when would you give montelukast

A

prevention and tx of chronic asthma
NOT for acute attacks

also can be used for
exercise induced asthma attack.
(must take at least 2 hrs prior to exercise)

114
Q

lifestyle modifications for asthma

A

reduce/avoid triggers of asthma attacks

  • keep windows closed during pollen season
  • keep home clean/reduce dust
  • reduce pet dander (hypoallergenic animal)
  • remove carpeting (carpet harbors dust)
  • cover nose and mouth in cold weather
  • control heartburn and gerd (medications)

use medications such as short term for acute attacks
and use long term meds to decrease risk of an attack

115
Q

what is COPD

A

a progressive pulmonary disease that is a combination of emphysema and bronchitis
characterized by persistent airflow limitation

116
Q

what is chronic bronchitis

A

the presence of excess mucous production in the lower respiratory tract

117
Q

how is chronic bronchitis diagnosed

A

when cough and bronchitis occurs for at least 3 months in a 2 year period

118
Q

what is emphysema

A

results from years of inflammation
loss of elasticity of bronchioles and damage alveoli
these alveoli collapse and trap air

causing decreased perfusion, decreased gas exchange

119
Q

what are the risk factors for COPD

A

exposure to cigarrette smoke
smoking any tobacco products
exposure to fumes, chemicals that can irritate and damage lung airways

120
Q

what are the treatments for COPD

A

we only have drugs to treat the symptoms we do not have any drugs to cure COPD

121
Q

what are the manifestations of COPD

A
  • chronic cough
  • sputum production
  • dyspnea(especially upon exertion)
  • barrel chest-from using more accessory muscles to breathe
  • wheezing
  • clubbed fingers
  • fatigue/weakness
  • activity intolerance
  • gas exchange abnormalities(retaining CO2)
  • increased susceptibility to infections which lead to COPD exacerbations
122
Q

what are lifestyle modifications for ppl with COPD

A
  • smoking cessation
  • avoid 2nd hand smoke
  • Breathing exercises
  • nutrition- (pts expel so much energy trying to eat) suggest higher caloric and protein but smaller meal
  • increase fluid intake(they become mouth breathers so they have dry mouth and loss of saliva. fluid also helps liquify sputum)
  • exercise- increases appetites, sleep and circulation
  • preventiontion-pneumococcal, flu vaccines
  • low level oxygen therapy
123
Q

what are breathing exercises for a COPD pt

A

teach them diaphragmatic breathing - using their belly to breath rather than their chest
and
pursed lip breathing to help expel as much CO2 as possible

124
Q

what is the goal for COPD oxygen saturation. what is specific about their drive to breathe

A

85-92%
as they get more severe, that o2 sat decreases a little
COPD pts depend on a hypoxic drive to breathe
(the body becomes accustomed to chronic CO2 retention- so eventually low levels of oxygen and high levels of co2 is their drive)

125
Q

what is the max amount of O2 you should give to a COPD pt

A

2L

126
Q

what is acetylcholine

A

released by the PNS

it binds to receptors on bronchial tree causing bronchiole constriction

127
Q

what is the short anticholinergic drug and what does it do

A

ipratropium inhaler

- it relieves and prevents bronchospasm of asthma and COPD

128
Q

what is ipratropium commonly used with

A

albuterol

for a nebulizer treatment

129
Q

what is the purpose of the duo neb

A

anti cholinergic response- decreasing constriction
and
beta 2 agonist response inhibits bronchodilation, decreases mucous production and inhibits release of inflammatory chemicals

130
Q

what is the long acting anticholinergic

A

tiotroprium
-dry powdered inhaler
dosed daily d/t long duration of action

131
Q

what is tiotroprium used for

A

maintenance and prophylaxis of bronchospasm for pts with COPD

132
Q

what is the adverse effect of anticholinergics

A

dry mouth

133
Q

what is the corticosteroid inhaler

A

fluticasone

-dry powder inhaler

134
Q

what does fluticasone do

A
  • anti-inflammatory
  • long term management of asthma or COPD
  • decrease edema and frequency and severity of asthma attacks
135
Q

what is advair

A

fluticasone AND salmeterol (long acting beta 2 adrenergic)

136
Q

what is the purpose of advair

A

decrease inflammation
to bronchidilate
and decrease mucous production

137
Q

how often is fluticasone/solmeterol used

A

twice a day

138
Q

what is Breo

A

fluticasone and vilanterol(beta 2 antagonist)

139
Q

how often is breo taken

A

once a day

140
Q

what are adverse effects of corticosteroid inhalers

A
  • headaches
  • hoarseness
  • oral/esophageal candidiasis (d/t corticosteroid)
141
Q

what do pts need to do after using corticosteroid inhaler

A

rinse mouth after each use and spit out. this will prevent oral/esophagela infections

142
Q

because fluticasone s a steroid what does the combo therapies increase the risk of

A

pneumonia and upper respiratory infections

b/c the steroid decreases the immune response to respond to inflammation

143
Q

what are systemic corticosteroids

A

methylprednisolone
and
prednisone

144
Q

what does methylprednisolone and prednisone do

A

help relieve airway inflammation
and act as anti inflammatory mediators so they inhibit the inflammatory response
decrease mucous production and edema

145
Q

what is a must do when stopping prednisone

A

it must be tapered down. do not abruptly stop because it can cause adrenal insufficiently

146
Q

what is adrenal insufficiency

A

this happens b/c the corticosteroids block the release of cortisol

147
Q

what are adverse effects of systemic corticosteroids

A 
hyperglycemia
euphoria
depression
HTN
decreased wound healing
ecchymosis
peptic ulceration
148
Q

what is different of the skin on a pt who has been taking a corticosteroids

A

they have very fragile think skin and the skin color turns brown

149
Q

what are pulmonary function tests used for

A

to evaluate lung function and diseases
used to assess air movement
-monitor disease progression
-monitor if med therapy is working and being effective

150
Q

explain the total lung capacity

A

the total amount of air that is in the lungs on maximal Inspiration
-how much air your lungs can hold

151
Q

what is residual volume

A

how much air remains in the lungs AFTER a pt expels the air

152
Q

what is the forced vital capacity

A
  • the amount of air that can be quickly and forcefully exhaled
  • measure how much air you can exhale before you need to take another breath
153
Q

what does the pH indicate

A

the concentration of H+ in our blood

154
Q

what are 3 mechanism to regulate acid base balance

A
  • buffer
  • respiratory
  • renal
155
Q

how does our body maintain pH by using buffers

A

bicarb and phosphate bind to acid to neutralize strong acids-reacts immediately

156
Q

how does respiratory system help maintain pH

A

lungs responsibility to breath in o2 and breathe out CO2

157
Q

how do the kidneys maintain acid base balance

A

if the body is acidotic
-kidneys reabsorb bicarb from tubule fluid and get rid of CO2

if the body is alkalotic
-the kidneys will get rid of bicarb and hold on to more H+

158
Q

what is the normal pH value
less than
greater than

A

normal
7.35-7.45
acidosis <35
alkalosis >45

159
Q

what is normal CO2 range
less than
greater than

A

35-45
>45- acidosis-hypoventilating
<35-alkalosis-hyperventilating

160
Q

what is the normal bicarb
less than
greater tahn

A

normal 22-26
<22-acidosis
>26 - alkalosis

161
Q

what are conditions of metabolic acidosis

A
  • diabetic acidosis
  • diarrhea-loss of bicarb
  • renal failure- kidneys not able to get rid of acid load so they retain H+, and not able to reabsorb bicarb
  • schock-d/t lack of blood flow
  • salicylate OD
162
Q

what are causes of metabolic alkalosis

A
  • loss of gastric secretions(losing stomach acid)
  • over use of antacids
  • K+ wasting diuretics (furosemide) because these diuretics cause K+ to be pulled out of cells and excreted so H+ enters the cell. (they switch places to maintain ion balance in cell) leading to alkalosis

202D (6 decks)

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