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3-Third semester > done-ChA exam 1- presentations > Flashcards

done-ChA exam 1- presentations Flashcards

1
Q

Body fluid balance

water in-where get 2.5 ml

water out-where 2.5 goes out

A

water in-2.2 food drink, 0.3l metabolism

water out-0.8 insensible loss(inc rr=inc loss), urine 1.5 l, feces .2 l

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2
Q

intracellular

A

Water inside the cells

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3
Q

extracellular

A

Water outside the cells:

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4
Q

interstitial

extracellular

A

Located in spaces between cells

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5
Q

intravascular

extracellular

A

plasma

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6
Q

trasnecullar

extraceullar

A

Other body fluid such as urine, digestive enzymes, & sweat

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7
Q

Osmosis-

process
water goes from
continues

A

primary process between icf and ecf compartments-

water moves from lower concentration to higher concentration

continues until both sides are equal

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8
Q

osmolarity

what is
number

A

concentration of a solution

number of solutes per kilogram

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9
Q

osmotic pressure

power

A

power of a solution to draw water across a membrane

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10
Q

Osmolality is determined by Na+ levels:

high

low

A

High Osmolality = High Na+
Low Osmolality = Low Na+

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11
Q

tonicity

effect

A

effect the osmotic pressure has on water movement across the membrane of cells within that solution

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12
Q

isotonic

A

same conectrstion as cells in plasma,

cells will not shrink not swell

ns and lr

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13
Q

Hypertonic-

A

cells will shrink due to water being drawn out of cell

3%

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14
Q

Hypotonic

A

Water moves into cell-cell expands

.45%

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15
Q

Diffusion-

A

molecules move from high concentration to low

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16
Q

simple diffusion

A

random movement of particles through solution

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17
Q

facilitated diffusion

A

uses proteins as carriers across membrane (glucose and amino acids)

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18
Q

Filtration-

A

water and dissolved substances move from area of high hydrostatic pressure to low hydrostatic pressure

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19
Q

where does filtration occur

A

kidneys

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20
Q

Active transport-

A

allows molecules to move across cell membranes and epithelial membranes against concentration gradient

requires ATP

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21
Q

Body Fluid Regulation: Thirst

primary
where is thirst center

A

Primary regulation of fluid intake.

Thirst center- hypothalamus

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22
Q

when is thirst stimulated

when what decreased
when what increases

A

Thirst is stimulated when blood volume decreases

serum osmolarity (concentration) increases

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23
Q

Kidneys functions

e

r

starts what

A

Excretion of water and electolytes

Reabsorption for regulating fluid/ electrolyte balance in body

Starts the Renin-Angiotensin-Aldosterone System

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24
Q

what happens in kidney failure

Fluid balance

A

gain more fluid

fluid can go to different parts of body and become overloaded

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25
Q

what happens in kidney failure

what goes up

what goes down

A

high-phosphate, fluid, potassium, magnesium

low-calcium

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26
Q

what causes RAAS to start

decreased, decreased, increased

Renin-angiotensin-aldosterone system

A

Decreased pressure,

decreased sodium delivery

and increased sympathetic delivery causes

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27
Q

Nephrons produce what

raas

A

renin

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28
Q

renin does what

goes where

changes to

A

which converts to angiotension 1

, goes to lungs,

changes to _angiotension 2

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29
Q

what is angiotensin 2

which does what

which then does what

A

__- a vasoconstrictor-

which increases BP and thirst,

which increase blood volume

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30
Q

angiotensin 2 stimulates what

to release what

A

and stimulates adrenal gland

to release __aldosterone__

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31
Q

aldosterone does what

leading to what

A

which increases Na and water retention,

leading to increased blood volume

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32
Q

RAAS simplified

kidneys
travels
this

A

Kidneys release Renin, converts Angiotensin I .

Travels to the lungs, meets ACE and change to Angio II (Potent vasoconstrictor).

This (Angio II), stimulates the adrenals to release aldosterone

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33
Q

Too much Angio II???

increases _arteries

increases resistance

remodeling of

A

Increases inflammation in the arteries-inc bp

Increases body’s insulin resistance

Remodeling of the heart muscle- the myocardium enlarges and also the conduction system is disrupted

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34
Q

what does too much angio 2 cause

A

hypertension

heart failure

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35
Q

Antidiuretic Hormone-

does what to water

A

reabsorption of water

save water and therefore less urine

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36
Q

when in ADH released

A

stress like pain, surgery, anesthesia

and low bv

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37
Q

when is ADH inhibited
a
m
increased
decreased

A

alcohol,

meds ,

increased blood volume

decreased serum somalaroty

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38
Q

Body Fluid Regulator - ANP BNP

opposes

inhibits

blocks

promotes

A

Opposes renin-angiotensin-aldosterone system

inhibits renin secretion,

blocks the secretion of aldosterone,

promotes Na+ loss and diuresis in the kidneys.

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39
Q

What do high levels indicate?

ANP BNP

A

cardiac stress

BNp could mean heart failure

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40
Q

Children
Percentage of water is _____
Metabolic rate is ____
Kidneys
Respirations are ____
Skin-

Risk for dehydration

A

Percentage of water is high

Metabolic rate is high

Kidneys are immature

Respirations are high

Skin-lose a lot of water from skin

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41
Q

FVD causes- Fluid loss examples

loss
h
h
med
__ disorders

A

GI loss (N/V/D, suction)

Hemorrhage

Heat (Exercise or environment)

Medications (Diuretics, laxatives)

Renal and endocrine disorders

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42
Q

FVD causes- poor intake examples

p l
decreased

A

Physical limitation

Decreased thirst mechanism

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43
Q

fvd causes- fluid shift examples

A

Second or Third spacing

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44
Q

FVD causes- older adults

renal
regulation
decreased
undetected
no
med use

A

renal blood flow decline,

NA, water regulation less efficient ,

decreased perception of thirst

, , undetected fever,

older adults with no air conditioning,

laxative use

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45
Q

Hypovolemia-

where is fluid drawn into

A

not enough fluid in patient

fluid is drawn into vascular compartment from interstitial spaces in attempt to maintain tissue perfusion

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46
Q

what fluid will you replace with in FVD

when to give blood in fvd

A

isotonic and blood

give blood if h/h under 7

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47
Q

second spacing

third spacing

what does it mean

-Fluid volume deficit-

A

2- shift of fluid to interstitial spaces

3-shift of fluid to transcellular spaces

trapped fluid is unable to support cardio/renal function

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48
Q

what is third spacing triggered by

increased

decreased

A

increased vascular permeability

decreased protein levels

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49
Q

why can second/third spacing cause fluid volume deficit

renal
leads to
allows

A

renal blood flow falls

leads to vasodilation

allows fluid to accumulate in interstitial tissues

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50
Q

s/s FVD

rapid
skin
tension
neck

A

rapid weight loss-2% mild,5% moderate, 8% severe

tenting skin turgor

postural/orthostatic hypotension

falt neck veins

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51
Q

Compensatory mechanisms to preserve circulation in FVD

cardia
skin
decrease
increase

A

tachycardia,

pale cool skin (vasoconstrictor )

decreased urine output

increase in specific gravity

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52
Q

older adults s/s FVD

changes

MM

increased
temp

cardia

facial

A

Change in mental status, memory or attention/

/ dry oral mucous membrane

, increased tongue furrows,

subnormal temperature,

tachycardia

pinched facial expression

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53
Q

FVD Diagnosis

Electrolytes- in isotonic// in water loss
Serum osmolarity
H&H-
Urine specific gravity-
Central venous pressure-

A

Electrolytes- in isotonic defeat-only sodium is normal// in water loss- sodium’s high

Serum osmolarity if water loss. High osmalarity

H&H-elevated

Urine specific gravity-increased

Central venous pressure-cvd decreased

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54
Q

FVD Assessment

assess for what

v
c
p p
daily
/
monitor lab

A

Assess for the clinical manifestations of FVD

VS-every 4 hours

CVP

Peripheral Pulses

Daily weight

I/O

Monitor Labs-electrolytes, serum omslaity, BUN

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55
Q

FVD Treatment: ORal

replace

if mild-

if more severe-

A

Replace gradually

If FVD is mild-
water

If FVD is more severe-
Water and electrolytes
sports drink, ginger ale or rehydrating

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56
Q

FVD Treatment: IV

may need when

what type of iv fluid

A

if severe and/or unable to drink

Lactated Ringer’s- Na+, K+, Cl-, Ca+, Mg+
0.9% NaCl (NS)

May need to add additional electrolytes

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57
Q

FVD- Treatments

Fluid challenge (Bolus)- what adminster
sees if what

Assessments we should be obtaining?

A

rapid iv infusion of isotonic solution

sees is cardiac/renal or if deficit

if in deficit vs will go back to normal

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58
Q

isotonic iv

types

what does

monitor for in all iv

A

NS, LR

same concentration as normal body

monitor for fluid overload in all iv solutions and disconrinue

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59
Q

hypotonic iv

types

what does

A

0.45 NS

Pulls water into cells
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60
Q

hypertonic

type
does what

A

-3% NS

, draws fluid from cells.

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61
Q

when to not adminster lactated ringers

what monitor with ringers

blood ph

A

do not administer lactated ringer in liver disease due to acidosis

if ringers are administered, monitor potassium and cardiac rhythm

do not administer if ph of blood is more then 7.5

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62
Q

when should d5w not be administered

A

for at risk cerebral edema

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63
Q

When to not administer hypotonic solutions

A

-do not adminster for at risk intracranial pressure-

do not administer for at risk third space shifts

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64
Q

risk for intracranial pressure

A

trauma, stroke, surgery

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65
Q

risk for third spacing shifts

A

-burns, trauma, liver disease, malnutrition

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66
Q

what to monitor for in hypertonic solutions

A

monitor for inflammation and infiltration- caused cells to shrink

monitor sodium levels

monitor circulatory overload

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67
Q

when to not adminster hypertonic solutions

A

diabetic ketoacidosis

impaired cardiac or kidney function

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68
Q

Nursing Interventions Dx- Deficit Fluid Volume
assess:-

&
assess
daily
administer/monitor
monitor
perfusion
safety issues

A

I&O-

Assess vital signs, CVP

Daily weight

Administer and monitor fluid intake

Monitor lab values-

Perfusion issues- kidneys, cerebral

Safety issues-change in LOC, dizziness, confusion, restlessness, anxiety

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69
Q

reducing risk for injury-

how to reduce orthostatic hypotension-

Fluid volume deficit

A

reduce risk for injury-safety precautions- bed in low position and slowly raising from supine to sitting/standing

tach how to reduce orthostatic hypotension-

move in stages
avoid prolonged standing
rest in recliner
use assistive devices to pick up

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70
Q

how to prevent fluid deficit

avoid
increase
if vomiting
reduce
importance

A

avoid exercising during heat

increase fluid intake in hot weather

if vomiting, rake small amounts of ice chips or clear liquids,

reduce intake of coffee, tea and alcohol

importance of maintaining fluid

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71
Q

when to see HCP

what will nurse do

Children With FVD

A

see HCP- Severe Vomiting and/or Diarrhea:

Replace fluids and treat the cause of diarrhea to minimize fluid loss.

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72
Q

measuring fluid intake in children–breasdtfed, weight

measuring fluid output in child -estimate, diapers

A

Fluid intake in child- breastfed in measured in minutes, weight before/after feeding,

Fluid output in child- estimate vomit output, diapers can be measured before/after,

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73
Q

enteral feeding in children why

A

Enteral feedings can be used in children because they help preserve stomach mucosa and have no risk of infiltration.

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74
Q

Mild dehydration s/s

r
v
t
/
fontanels
has

dehydration in children

A

restless,

vs,

turgor

, u/o,

fontanels normal,

has tears.

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75
Q

Moderate dehydration s/s children

I
l
_tensive
_cardic
skin
__mucous membranes
decreased__
__fontanels

A

irritable,

lethargic,

hypotensive,

tachycardic,

poor skin turgor,

dry MM,

decreased tears,

sunken fontanels.

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76
Q

Severe dehydration s/s children

no
no
pulse

A
  • no urine,

no tears,

rapid weak pulse

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77
Q

Prevention- dehydration in children

proper
safe
safe

A

proper clothing,

safe isolette temp,

safe exercise

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78
Q

rehydration- in children
types
amounts
ex
avoid

A

PO or IV

Small, frequent amounts

Ex. Clear liquids, pedialyte

Avoid concentrated simple sugars due to osmotic affects

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79
Q

what to do if Diarrhea >24 hour in children

A

– stool cultures (may need antibiotic)

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80
Q

Elderly With FVD

not reliable
tension
mucous
changes in

A

Skin turgor not a reliable sign

Orthostatic hypotension

Dry mucous membranes

Mental status changes

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81
Q

FVE

results when

can lead to

A

Results when water and sodium are retained in body

can lead to hypervolumia and edema

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82
Q

causes of FVE

failure
cirrhosis
failure
disorders
administration

A

heart failure

liver cirrhosis

renal failure

adrenal gland disorders

corticosteroid administration

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83
Q

Nuerlogic manifestations of FVE

4

A

changes in loc

confusion

headache

seuizures

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84
Q

respiratory manifestations FVE

A

pulmonary congestion-crackle sin lungs

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85
Q

cardiosvasular manifestaitons in FVE

incresed x3
presence
cardia

A

increased bounding pulse

increased bp

increased JVD

presence of s3

tachycardia

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86
Q

gi manifestaitons inFVE

A

anorexia

nausua

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87
Q

edema in FVE

A

dependent pitting edema

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88
Q

s/s of FVE

A

Weight

Respiratory

Urine output

Edema

Altered mental status

Cardiac

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89
Q

FVE: Diagnosis
Electrolytes

H/H-

Renal function-

Liver function-

Urine specific Gravity-

A

Electrolytes- normal

H/H- decreased

Renal function- determani cause

Liver function- determain cause

Urine specific Gravity- decreased

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90
Q

complications of FVE

A

CHF

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91
Q

Assessment of FVE: History

A

Medications

Medical
-Heart failure
-Kidney disease
-Liver failure

Diet

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92
Q

medications in FVE

A

diretics

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93
Q

loop diretics

what type
promotes what
works where

A

-ide” like bumetanide furosemide /

/promote excretion of sodium, chloride, potassium and water-

worls on loop of henle//

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94
Q

Thaizade-
ends in what
promotes what
woks where

A

ends in thiazide-

promote excretion of sodium, chloride, potassium and water by decreasing absorption-

works on dital convoluted tubule

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95
Q

potassium sparing-

works where
what drug
promotes what

A

worls on distal nephron,

spironolocatone,

promotes water echange and inhibits potassium

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96
Q

Fluid management- FVE

subtract
palce
offer
give
adminster

A

subtract required fluid from total daily allowance/

place allowed amounts in small glasses/

offer ice chips/

sugarless chewing gum/

admisnter cautoisly

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97
Q

dietary management FVE

avoid——

A

LOW sodium

avoid lunch meat, bacon, cheese, dry cereal. canned soup. popcorn, ketchup, pickles seafood

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98
Q

reduce risk of skin breakdown

assess
reposition. how often

what helps

and oral care how often

A
  • asses bony provinces,

reposition every 2 hours,

egg crate mattress, alternating pressure mattress, foot cradle, heel protector,

Oral Care-e very 2 hours

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99
Q

Patient education//Diretics-

dont take
make
avoid
daily
no

always

replace

A

don’t take at night,

make slow positional changes,

avoid salt,

daily weights,

no salt substatiuts in potassium sparing

reports dizziness

always taken

replace potassium with orange juice and banana

100
Q

management of FVE

daily
assess extent
urine
assess v
assigns lungs

A

daily wights

assess extent of edema

assess urine output

assess vitals

assess lungs for crackles

101
Q

FVE in children causes

tumor
c
l
failure

A

adrenal tumor,

CHF,

liver

renal failure

102
Q

FVE s/s children

sudden
edema where

A

S-sudden wt. gain,

edema in dependent areas (sacrum, genitals)

103
Q

FVE in risk factors children

A

rapid iv infusion

104
Q

Sodium

major

NA=

critical level

increased sodium=

A

Major Electrolyte

Na+ = Neuromuscular

critical level is under 120

increased sodium = increased water retention

105
Q

what happens to cells when sodium levels are low

when high

A

When sodium levels are low (hyponatremia), water is drawn into the cells of the body, causing them to swell. hyponatramia= hypervolemia

In contrast, high levels of sodium in ECF (hypernatremia) draw water out of body cells, causing them to shrink//hypernatramia=hypovolemia

106
Q

How much do we need daily sodium

where is intake most common w/ other sources

A

500 would meet needs, intake of no more then 2300, with ideal of 1500 mg

Intake:
Most common: dietary
Other sources: meds

107
Q

primary regulator of sodium

A

kidneys

108
Q

GFR goes up wen

A

when there’s a rise in blood volume

rise in fitler rate

109
Q

when blood volume falls, what is stimulates

A

RAAS and ADH

110
Q

hyponatrimai patho- from hypovolemia

gi-
skin-
adrenal-
med type
iv solution

A

GI-N/V/D, NG suction

Skin-sweat, wounds, burns

Adrenal insufficiency-Addisons

Diuretics

Hypotonic IV Solution (Na goes into the cell)

111
Q

hyponatrmia from hypervolemia

excess
S
systemic diseases-

patho

A

Excessive H2O intake

SIADH-body retains fluid

Systemic diseases- heart failure, renal failure, cirrhosis of liver

112
Q

early manifestations of hyponatramia

3x
gi-4x

A

muscle cramps

weakness

fatigue

gi- anorexia, nausea, vomiting, abdominal cramping

113
Q

nueroligcal manifestations of hyponatramia (<120)

h
d
duled
changes in
I
L
refelxes
mt
s

A

headache

depression

dulled sensorium

personality changes

irritibiltiy

lethargy

hyperreflexia

muscle twitching

seizures

114
Q

manifestations of hyponatramia

in decreased ECF volume

in dilutional

A

decreased ecf volume- s/s FVD-

dilution- s/s of hypervolemia

115
Q

severe loss of sodium leads to what

A

coma due to cerebral swelling

116
Q

Hyponatremia- Diagnostic tests

serum sodium/osmalarity

24 hr urine-
in increased volume, in loss of fluids

A

Serum sodium- decreased

Serum osmolarity- decreased

24 hour urine specimen-in increased volume- sodium high,
in loss of fluids- sodium decreased

117
Q

hyponatremia Interventions
hypovolemia

replace
diet

A

Replace with isotonic solutions

Diet- increase Na+

118
Q

hyponatremia Interventions
hypervolemia

meds
fluids
diet

A

Diuretics furosemide to get rid of fluid

Fluid Restriction

Diet- increase Na+

119
Q

hyponatremia Interventions
if severely low-110-115

what oral
and what iv fluid
need what if iv

A

Sodium tablets

3% hypertonic NaCl (Na+ 110-115 mEq/L) – administer cautiously

need central line

120
Q

Clients At Risk hyponatramia

A

Athletes
Workers
Elderly
Children

121
Q

Nursing Interventions for Imbalanced Fluid Volume

monitor
daily
24
could be

hyponatramia

A

Monitor I & O,

daily weight,

24 hour fluid balance

could be FVE or FVD

122
Q

Nursing Interventions for Imbalanced Fluid Volume
iv fluids-monitor for wgat
bp
c
h
r
d
c

what if ordered

A

carefully monitor for Fluid volume excess
Hypertension
, CVP
, HR
, RR,
Dyspnea,
crackles

Fluid restriction if ordered

123
Q

Nursing Interventions for Imbalanced Fluid Volume

Monitor for s/s of ineffective cerebral tissue perfusion-
na 115-120

na 110-115

A

assess neurologic changes and muscle strength

Na+ 115-120- Headache, lethargy

Na+110-115- Seizures, coma

124
Q

hyponatramia education

fluids
manifesations
older adults

A

increase fluids containing sodium

manifestaitons to report to hcp,

older adults have increased risk from medications.

125
Q

Hypernatremia causes MODEL

A

M- Medication

O- Osmotic diuresis

D- Diabetes Insipidus

E- Excessive water loss

L- low water intake

126
Q

hypernatramia also caused by

excess

h/b

excess

A

excess iv fluids and food

hyperventilation/burns

excess water loss from watery diarrhea, fever

127
Q

Patho of Hypernatremia

A

Hyperosmolarity-

Cells shrink  cell dehydration

128
Q

initial s/s hypernatramia

first-

if not releived- primary manifestations are
l
w
i

A

thirst,

if not releived
lethargy,
weakness
irritable

129
Q

prolonged s/s hypernatramia

s
c
d

potentially complications

A

seizures,
coma,
death

130
Q

brain cell

both

na

A

Brain cell dehydration leads to bleeding.

Both high or low N+ lead to cognitive issues.

131
Q

Hypernatremia: S/S

increased
decreased
dry
h
r
s
cardia
tension

A

Increased thirst

Decreased urine output

Dry skin and mucous membranes

Headache,

restlessness

Seizures

Tachycardia

Hypotension

132
Q

Diagnosis of Hypernatremia

A

Serum sodium level- over 145

Serum osmolarity- high

133
Q

Hypernatremia Assessment

health history
physical
diagnostic tests

A

Health history-
precipitating factors, current medications, perception of thirst

Physical-
Vitals
LOC
I&Os

Diagnostic tests-
Na+, osmolality

134
Q

Medication Treatments hypernatrmia
‘
main treatment?
how fast
what iv fluids-
what meds-

A

Main treatment: replacing with fluids

SLOWLY

What type of IV fluids? hypotonic

Diuretics? Can increase sodium excretion-add fluids

135
Q

Interventions for Risk for Injury hypernatramia

monitor/maintain
monitor _function
institute
re
monitor for

A

Monitor and maintain fluid replacement

Monitor neurologic function

Institute safety precautions as necessary- keep bed low and side rails up

Reorient

Monitor for Seizures-

136
Q

hypernatramia education

importance of

following

importance

A

Impirtance of responding to thirst and consuming adequate fluids,

following a low soidum diet,

imprtance of monitoring levels

137
Q

Potassium-

major
essential
ompacts

A

Major electrolyte within the cells

Essential for cardiac and neuromuscular function

Impacts pH

138
Q

potassium foods

A

Must be obtained in food daily
bananas

iranges

avocados

spinach

potatoes

meat

seafood

milk

139
Q

potassium regualtion-High K+ in serum

A

Increase the Aldosterone release

Kidneys increase K+ excretion

140
Q

potassium regulation low k

A

Nothing happens: Kidneys do not conserve K+ well

141
Q

Renal Failure and K+

A

impaired renal excretion of potassium is primary cause of hyperkalemia

142
Q

Hypokalemia causes

excess
losses
meds-3
loss
reduced

A

Excessive loss of K+

GI losses- diarrhea, ileostomy drainage

Medications- Diuretics-corticosteropids, antibiotics

Renal Loss

Reduced K intake

143
Q

Manifestations of Hypokalemia

ECG changes-

Muscles-

secretion//high

urine

A

ECG changes-depressed ST, U waves

Muscles- leg cramps

decreased Insulin secretion-glucose is high

dilute urine

144
Q

urinary 3

manifestations of hypokalemia

A

-dilute urine,

polyuria, -excess urine production

polydipsia-excess thirst

145
Q

gi

/
a
d
bowel sounds
i

manifestations of hypokalemia

A

n/v

anorexia

diarrhea

decreased bowel sounds

lieus

146
Q

musculoskeletal

f
cramps where
m w
poor

hypokalemia

A

fatigue

leg cramps

muscle wekaness

poor muscle tone

147
Q

cardiovascular

d
pulse
p h
risk

hypokalemia

A

dysthymia’s

irregular weak pulse

postural hypotension

increased risk of dig toxicity

148
Q

Diagnosis of Hypokalemia

Serum potassium-
mild
moderate
severe

ABGs-

Renal function studies-

ECG

A

Serum potassium-
3-3.5- mild
2.5-3- moderate
< 2.5mEq/L- severe

ABGs- alkalosis-pH increased >7.45

Renal function studies- check creatinine and BUN, GFR

ECG–depressed ST, U waves

149
Q

complications of hypokalemia

A

resp arrest

cardiac arrest

150
Q

Hypokalemia - Assessment

health history
physical
test
assess for causes

A

Health history-
current manifestations, duration, current meds, diet

Physical-
LOC changes, VS, pulse, decreased BS, muscle weakness, nausea, vomiting, abdominal pain

Diagnostic tests

Assess for causes-
diuretics, prolonged N/V/D or chronic

151
Q

Assessments for Hypokalemia

monitor what

assess ecg-what looks like

how is pulse

check levels of what

muscle strength

bowel sounds

pain where

A

Monitor serum K levels

Assess VS and ECG- depressed ST, U waves

  • thready pulse, weak

Check digoxin levels

Muscle strength weak

Bowel sounds hypoactive

Abdominal pain

152
Q

oral supplements
dilute
give-why
give

Hypokalemia IMMEDIATE Interventions

A

dilute oral in vegetable juice/

/ give oral with food-can cause gi upset

give chilled

153
Q

iv supplements -potassium chloride

infuse rate
no
no
monitor
give where if possible

Hypokalemia IMMEDIATE Interventions

A

infuse at rate slower then 10 meq//

no iv push

no undiluted

cardiac monitoring

give in cvad is possible

154
Q

hypokalemia

digitalis toxicity

A
  • fatigue,

weakness,

hypotension,

nausua

155
Q

Hypokalemia Long Term Interventions

dont take what in potassium sparing diuretics

when to take potassium supplements

diet

do not w/ tablets

A

Do not take potassium supplements or salt substitutes if also taking potassium sparing diertic,

take potassium suplemetns woth meals,

high potassium diet,

do not chew coated tablets,

156
Q

Hyperkalemia- causes

main
disease
inadequate
meds 3x
a
rapid

A

Main: Renal failure/Impaired excretion

Addison disease

Inadequate aldosterone

Medications- Potassium sparring diuretics- ACE(pril) I- ARBs(artan)

Acidosis

rapid iv administration

157
Q

early manifestations of hyperkalemia

d
cramps where
a
p
I
m t
t

A

diahhrea ,

colic-ab cramping-pain in waves

anxiety

parestheasas

irritability

muscle tremors

twitching

158
Q

later s/s of hyperkalemia

muscle//progresing
(what’s affected first)

hr

A

muscle weakness progressing to paralysis

lower extremities affected first

hr bradycardia and irregular

159
Q

what do t waves look like in hyperkalmia

A

tall t waves

tombstone t

160
Q

Diagnosis of Hyperkalemia

serum electrolytes
ABG
ECG

A

Serum electrolytes- potassium over 5.3, low calcium and sodium

ABGs- determnain acidosis

ECG- peaked t waves,prolonged pr and qrs

161
Q

Hyperkalemia complications

A

dysrtymias

162
Q

Medications to Correct Hyper K+

what helps for 1 hr
what rapidly lowers levels
s
d

A

Calcium gluconate-helps for 1 hr

Insulin, glucose, sodium bicarb IV- montor bradycardia

Sodium polystyrene sulfonate-monitor sodium and poop

Diuretics-furosemide

163
Q

when do you give diuretics in hyperkalemia

A

only if real function is normal

164
Q

when dialysis in hyper kalmia

A

When renal function is severely impaired and other measures are ineffective.

165
Q

what education in hyperkalemia

monitor repose

diet

avoid

A

Monitor response to iv calcium gluconate- calcium can increase digitalis toxocity

Diet and restrict salt substituts and high potassium foods

Avoid fitness and over the coutner supplements

166
Q

Calcium Imbalance

sources

where is calcium

A

Sources-

99% of all body calcium is in skeleton

167
Q

what % in body// where bound to

bones

bound extraceullar

ionized extracellular

A

bones -99%/phosphorus

bound extraceullar ions.5% proteins

ionized extracellular .5% nothing

168
Q

Calcium helps with:

stablizes
muscle
function
blood

A

Stabilizes cell membranes

Muscle contractions

Cardiac function

Blood clotting

169
Q

parathyroid gland
when ca is what

increases reabsorption where
increase absorption where
increase what reabsorption
increase what levels

Balance of Calcium in Body

A

When Ca is low:

Increases bone reabsorption (release to blood)

Increases GI absorption

Increases tubular reabsorption

Increases serum calcium levels

170
Q

calcitonin
when ca is what

released by

oposes

decerases absoption

increases mineralization

promotes

decreases what

Balance of Calcium in Body

A

When Ca is high:

Released by thyroid gland

Opposes parathyroid hormone

Decreases GI absorption

Increases bone mineralization

Promotes renal excretion

Decreases serum calcium levels

171
Q

Balance of Calcium in Body Calcitriol

metabolite of what
increase bone
increase absorption
increase reapportion
increase levels

treats low calcium in what

A

vit d metabolite

Increases bone release to blood

Increases GI absorption

Increases tubular reabsorption in kidneys

Increases serum calcium levels

treats low calcium in kidney disease

172
Q

Hypocalcemia-causes

H
acute

A

: hypoparathyroidism,

acute pancreatitis

173
Q

Hypocalcemia- risk factors

p
intoleracne
adults
a
med

A

: parathyrodectomy ,

lactose intolerance,

older adults,

alcoholism

diuretic usage

174
Q

neurological manifestations hypocalcemia

most serious-2

What/where

dtr

+

A

most serious -tetany/convulsions

Numbness and Tingling - Face (mouth Hands and feet

dtr hyperactive-

positive C/t

175
Q

cardiovascular manifestations hyocalcemia

tension
cardia
vd

A

hypotension

bradycadia

ventrilar dystrymias

176
Q

CATS of Hypocalcemia

A

C-convlusions
A-arrhythmias
T-tetany
S-spasms and stridor

177
Q

complications of hypocalcemia

ao

vd

ECG

ca

A

airway obstruction- largyngospasm (emergency

ventricular dystrymias

prolonged qt intervals

cardiac arrest

178
Q

Diagnosis of Hypocalcemia

Total serum calcium-
Serum albumin-
Serum magnesium-
Serum phosphate-
Parathyroid hormone-
ECG-

A

Total serum calcium- low
Serum albumin-low
Serum magnesium-low
Serum phosphate-high
Parathyroid hormone-low
ECG-prolonged qt

179
Q

Interventions for Hypocalcemia tetany

A

provide a quiet environment

institute seuizure precautions

airway at bedside

180
Q

Oral calcium hypocalcemia

administer when

give with

also give

A

administer 1-1.5 hours after meals and at bedtime

/ give with water and not milk

also give vit d

181
Q

IV calcium hypocalcemia

why is it used

given how fast

adminster where

do not adminster with

A

used to prevent life threatening airway obstruction

may be given by slow iv push

, adminster in largest vein,

do not admisnter with sodium bicarb

182
Q

potential problems with iv calcium

if infiltrated

if too rapid off drug administration

A

Iv calcium can cause necrosis and sloughing of tissue if infiltrated into subcutaneous

Rapid drug administration can lead to bradycardia and possible cardiac arrest due to overcorrection

183
Q

hypocalcemia education

maintain

calcium carb can cause

A

, maintain adequate vit d intake,

calcium carbonate can cause constipation -eat high fiber diet.

184
Q

Hypercalemia- > causes

2most common
hyper
m

rest
failure
increased
excessive

A

2 most common
Hyperparathyroidism

malignancies

Bed rest

Renal failure-

Increased Vit. D intake

Excessive intake (antacids)

185
Q

Muscle- Manifestations of Hypercalcemia

2

A

muscle weakness

fatigue

186
Q

GI Manifestations of Hypercalcemia

A

-anorexia
nausea
vomitong
consitaption

187
Q

CNS Manifestations of Hypercalcemia
5

A

-difficulty concentrating
confusion
lethargy
behavior changes
coma

188
Q

Cardiac–Manifestations of Hypercalcemia
3

A

dysrthmias
ecg changes
hypertension

189
Q

complications of hypercalcemia

disease
p
excess
kindey

A

peptic ulcer disease

pancreatitis

excess calcium

kindly stones

190
Q

Diagnosis of Hypercalcemia

serum calcium
serum PTH
ECG
why bone density

A

Serum electrolytes- high calcium

Serum Parathyroid hormones-high

ECG- shortened st

Bone density-monitor bone reaboption

191
Q

Medications/ Fluid Management hypercalcemia

main one

diretic// when

emergency reversal

what iv fluid

A

Calcitonin-

Diuretics- furosmemide// in acute

IV sodium or potassium phosphate- emergency reversal

isotonic iv fluid

192
Q

what drugs are used in malignant hypercalcemia

A

“ate” drugs

bisisophanates-

pamidronate

etidroante

193
Q

hypercalcemia

diet

type of iv fluid

drink what

A

Low calcium diet

Isotonic IV fluid

drink cranberry juice

194
Q

what puts them at Risk for injury- hypercalcemia

c
precutions-when
w/

caution-why

A

confusion,

safety precautions if changes in mental status

weak/ fatigued

caustion with turning postioning and ambulating- have weak bones in reabsorption

195
Q

Risk for excess fluid volume- hypercalcemia

in what//whose at risk
+
sounds
__up
meds

A

-renal failure

, I+O,

heart and lung sounds,

HOB up,

diuretics

196
Q

education in hypercalcemia

avoid
increase
maintain
hypercalcemia can cause

A

avoid intake of calcium rich foods/antacids

increase fluid intake to 3-4

maintain weight bearing physical activity

Hypercalcemia can cause bradycardia, cardiac arrest,

197
Q

function of mamgensium

reactions
synthesis

where is most

A

enzyme reactions

synthesis of proteins and nucleic acids

in the bone

198
Q

dietary sources magnesium

A

green vegetables

seafood//meats

nuts

milk

199
Q

Hypomagnesemia- < 1.8 mg/dL

common problem for who

may be caused by//deficent, excessive,

d

d

A

Common problem for critically ill

May be caused by deficient intake, excessive losses or shift from extracellular to intracellular

dka

diretics

200
Q

hypomagnesemia risk factors

loss
e
m
d

A

loss of gi fluid

ETOH

malnutrition

diuretics

201
Q

Neuro muscular

-Manifestations of Hypomagnesemia
6

A

tetany,

seizures

hyperactie reflexes,

positive chovestek and trousseau ,

nystagmus-twitching og eyeball

-tremors,

202
Q

cardiac Manifestations of Hypomagnesemia

2

A

hypertension
tachycardia

203
Q

cns Manifestations of Hypomagnesemia

4

A

confusion

mood changes

hallucinations

possibl;e psychoses

204
Q

treatment hypomagnesemia

mild deficiency treated with what

A

mild- oral magnesium and diet of high magnesium

205
Q

diagnosis hypomagnesemia

A

prolonged pr interval,
widened qrs complex,
depression of st

206
Q

treatments hypomagensmia if manifestations

treated with

what to do before that

adminster im where

A

treated with parenteral magnesium sulfate-

evaluate renal function prior to administration-

administer im into ventral gluteal and monitor neurologic status

207
Q

Hypermagnesemia-

how common

develops when

with what meds

A

less common

renal failure

laxatives

208
Q

lower levels-
/
tension
face
s
feeling

Manifestations of Hypermagnesemia

A

n/v,

hypotension

, facial flushing,

sweating

, feeling of warmth

209
Q

as levels increase

hypermagnesemia

A

lethargic

drowsiness

weka/absent dtr

210
Q

marked elevation of magnesium

potential complications -3

hypermagnesemia

A

resp distress

coma

compromised cardiac function

211
Q

Hypermagnesemia Interventions

stop
d
iv what

A

Stop magnesium containing medications

Dialysis

IV calcium gluconate-reverses neuromuscular and cardiac effets

212
Q

monitor for

decrease-may need
ineffective-may need
risk

Hypermagnesemia Interventions iv calcium gluconate

A

decreased cardiac output (may need pacer)

ineffective breathing patterns (may need vent)

risk for injury

213
Q

Phosphate Imbalance

essential for what

and formation

__function/metabolism

A

Essential for intracellular processes like ATP-

RBC formation,

nervous system and muscle function and metabolism

214
Q

calcium and phosphate relationship

A

as one goes down one must go up

215
Q

Hypophosphatemia- < 3 mg/dL causes

syndrome
meds
a
ventilation
a

A

refeeding syndrome

meds like iv glucose

alchohism

hyperventilation-
alcohol

216
Q

CNS Manifestations of Hypophosphatemia

I
a
w
p
lck
c
s
c

A

irritability,

apprehension,

weakness,

paresthesias,

lack of coordination

, confusion,

seizures,

coma.

217
Q

Hematologic

cardiac

gi-decreased,anv.

Manifestations of Hypophosphatemia

A

Hemolytic anemia (excessive RBC destruction) may develop due to lack of ATP -

cardiac-chest pain -dystrhmias

gi- anorexias, nausua/ vomiting, decreased bowel sounds

218
Q

Musculoskeletal- Manifestations of Hypophosphatemia

weakness
release
acute

A

muscle weakness,

release of CPK,

acute rhabdomylosis

219
Q

Interventions hypophophatemia

Dietary

Medications

Monitor for?

A

Dietary - high phosphate

Medications oral phospahte

Monitor for? seizures and coma

220
Q

foods high in phphate

A

meat

dairy

nuts

221
Q

Hyperphosphatemia- causes

failure of

rapid

shift of

altered- excess

A

Acute or chronic renal failure-

Rapid administration of phosphate containing solutions

Shift of phosphate from intracellular to extracellular

Altered calcium levels- excess vit d

222
Q

Manifestations Hyperphosphatemia

5

A

muscle cramps and pain,

paresthesias,

tingling around the mouth,

muscle spasms,

tetany)

223
Q

Interventions hyperphosphatemia

treat

monitor

A

treat underlying disorder

monitor for hypocalcemia

224
Q

Chloride

cellular
works with
part of
n
is apart of
imbalance is caused by

A

Extracellular

Works with sodium

Part of HCL

Normal

Cl- is part of salt

Imbalance caused by other imbalances like Na+ and corrected by fixing the other imbalance

225
Q

Diabetes Insipidus

Result

renal tubules

neurogenic
nephrogenic

A

Result of ADH insufficiency

renal tubules are not sensitive to ADH

neurogenic is cause from hypothalamus and nephrogenic is caused from renal tubules not being sensitive

226
Q

Who is at risk for developing?

brain
surgery
accidents
failure
closed

Diabetes Insipidus

A

– brain tumors /infections,

pituitary surgery,

cerebrovascular accidents,

renal/organ failure.

closed head trauma w/increased intracranial pressure

227
Q

Diabetes insidious manifestations

large
p
d w/

A

large amounts of dilute urine(12)L,

polydipsia-extreme thirst and drinks large water,

dilute w/ low specific gravity urine

228
Q

diabetes insidious

What diagnostic tests would be performed?What results would be expected?-

sodium
serum osmolarity
specific gravity

A

hypernatremia,

high serum osmolarity,

low specific gravity

229
Q

What are the potential complications? diabetes insidious

A

If patient is unable to replace water loss they get dehydrated and hypernatremic,

230
Q

What treatments/interventions would be used to treat (including diet and medications)?-

initally

replacing

what iv if high sodium

what do if high sodium

A

initially correcting fluid deficits,

and replacing ADH with vasopressin

hypotonic solutions are used if sodium is high

seizure precautions id sodium is is high

231
Q

Syndrome of Inappropriate Anti-diuretic Hormone-

high levels

water
urine

A

high levels of ADH

water retention

small amounts of concentrated urine output

232
Q

Syndrome of Inappropriate Anti-diuretic Hormone-

l/h

injury
disease
adverse reaction

whose at risk

A

lukemia and hodkpngs lymphona

heda injury

pulmonary disease

adverse reaction of sari

233
Q

Syndrome of Inappropriate Anti-diuretic Hormone-

diagnostics

sodium
osmoloarity
specific gravity

A

low sodium,

low osmolarity,

high specifc gravity

234
Q

Syndrome of Inappropriate Anti-diuretic Hormone- manifestations

urine- output/c
natramia
fluid w/
changes
wt w/

A

Hyponatremia-

fluid retention with thirst ,

decreased urine output and concentrated urine,

mental status/personality Changes,

Weight gain w/ no edema

235
Q

Syndrome of Inappropriate Anti-diuretic Hormone-What are the potential complications?

too rapid
what if hyponatramia

A

Too rapid replacement of sodium can case demyelination of central nervous system

seizures if hyponatremia is severe leading to cerebral edema

236
Q

Syndrome of Inappropriate Anti-diuretic Hormone-interventions

restrict
keep
med
iv fluid

A

Restrict fluids,

keep patient safe /

/ loop diuretics-excretion of fluid volume//

iv hypertonic solution if severe

237
Q

Adult with Gastroenteritis
Who is at risk for developing?

A

Goes in body through food, no real risks for anyone

238
Q

Adult with Gastroenteritis manifestations
a
n
d
ab
bowel//and
sounds

A

Anorexia/ n/v,
diarrhea

abdominal discomfort,

bowel distention and tender,

loud and hyperactive sounds

239
Q

Adult with Gastroenteritis- diagnostics

lab testing

sigmoidoscopy why

A

lab testing to causative organism and to assess fluid electrolyte imbalance. ,

sigmoidoscopy to differentiae ibd from infections

240
Q

Adult with Gastroenteritis- complications

A

electrolyte imbalances- hypos

hypovoemiv shock

241
Q

Adult with Gastroenteritis interventions

should

if manifestations

replacing fluids->

precautions

A

Should resolve on own, so no meds required unless severely ill or prolonged

manifestations- then look for “mycin” antibiotics- need stool culture first. /// antidiarrheal promote comfort

replacing lost fluids-> oral rehydration

iso precautions

242
Q

Adult with Gastroenteritis

if getting culture

importance of

wash

importance of
dont leave

A

If getting stool culture, use clean bedpan and avoid urine and toilet paper if possible to get best results

importance of hand hygiene,

wash clothing and linens, oral solutions,

, importance of proper food handling

,don’t leave dairy products or egg products at room temperature

243
Q

Metabolic acidosis-

inc
urine
results from

A

inc respirations,

acidic urine,

results from diahhrea because lots of sodium is lost

244
Q

Metabolic alkalosis-

from
what’s lost
respirations

A

from vomiting,

chl is lost,

slow respirations,

245
Q

why not hypo/hyper fast administration

A

can cause fluid shifts that will overcorrect

3-Third semester (13 decks)

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