X Fluid & Electrolytes Flashcards

1
Q

Only administer Insulin in ….

A

an Insulin syringe

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2
Q

IM injections given at ? degrees

A

90degrees

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3
Q

Heparin used for?

A

Anticoagulant

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4
Q

do not aspirate Heparin or Insulin

A

??? WHY

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5
Q

Recombinant DNA

A

DNA made in the lab by combining different genetic material from multiple sources, creating sequences that would not otherwise be found in biological organisms.

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6
Q

ADH released by pituitary in response to …

A

thirst or concentrated blood. stops kidneys from producing urine

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7
Q

Solutes (glucose, protein, NaCL) in blood attract….

A

H2O

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8
Q

Diabetes Insipidus causes

A

polyurea

fluid passes thru to quickly. dilute urine

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9
Q

SIADH

A
  • Syndrome of Inappropriate ADH.
  • Body produces too much ADH. Kidney gets message to pull back fluid too much.
  • Urine [ ], DWN urine output, UP BP, edema w/ fluid seeps into interstitial space
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11
Q
RAAS system
(Renin Angiotensin Aldosterone System)
A
  • Renin secreted by JGA in response to Low BP
  • Renin enters blood stream, causes conversion of Angiotensinogen to Angiotensin I
  • Angiotensin I (in lungs) converted to Angiotensin II (vasoconstrict)
  • Angiotensin II stimulates release of Aldosterone from Adrenal Cortex. (signals kidney to pull back Na, then fluid)
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12
Q

ACE inhibitor

A

Angiotensis Converting Enzyme. Given to patients who release to much and HTN
(blocks conversion of Angiotenisin I to II)

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13
Q

ANP

A

Atrial Natriuretic Peptide

  • released in response to overstretching of Atria during fluid overload.
  • Tells kidney to release Na and let o of water to decrease water.
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14
Q

BNP

A

Brain Natriuretic Peptide

-secreted by the ventricles of the heart in response to excessive stretching of heart muscle cells (cardiomyocytes)

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15
Q

LOW BP, LOW BV, UP Blood Osmolality

then ADH =

A

UP BP, UP BV, LOW Blood Osmolality

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16
Q

Aldosterone released (by Adrenal Cortex) in response to ….

A

UP K.

if kidney normal, high K indicates dehydration

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17
Q

ADH deals with H2O, Aldosterone deals with ?

A

solids, (K)

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18
Q

Serum Osmolality & Specific Gravity indicates ? about kidneys

A
  • how effective kidney is at producing urine

- if serum UP, USG usually UP too.

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19
Q

Filtration: Hydrostatic pressure does ?

A

pushes fluid out of artery

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20
Q

FIltration: Osmotic pressure does?

A

attracts fluid back into veins. Excell fluid picked up by Lymph or it will cause edema.

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21
Q

All plasma protein made ?

A

Liver

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22
Q

Hypervolemia symptoms

A

Na & H20 retention

  • bounding pulse
  • tachycardia
  • UP resp rate
  • Distended neck veins
  • UP BP
  • Heart failure
  • Weight gain
  • crackles
  • Osmolality DOWN
  • U Specific Grav DOWN
  • Fluid retention
  • HTN
  • DOWN HCT
  • dependent edema
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23
Q

Hypovolemia

A

decreased BV

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24
Q

Hypovolemia Causes

A
  • 3Ds (diarrhea, diuresis, diaphoresis)
  • internal bleeding
  • obstetric emergency
  • dehydration
  • vomit, fever
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25
Q

Hypovolemia Symptoms

A
tachycardia 
weak/thready pulse
anxiety/confused thinking
fatigue
weight loss
DOWN BP
dry skin/mucous membrane
poor skin turgor
[ ] dark urine
risk for fall (orthostatic hypotension)
risk for skin breakdown
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26
Q

Leading cause of hospital admissions?

A

Dehydration, Hypovolemia

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27
Q

Hypovolemia Treatment

A

restoring BV???

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28
Q

Hypovolemia (dehydration), Nursing Implications

A
  • Acute renal failure
  • coma
  • shock
  • osmolality UP
  • hematocrit UP
  • BP DOWN
  • Urine SG UP
  • dry mucous membrane
  • poor skin turgor
  • ADH released
  • thirst
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29
Q

Isotonic solution in veins

A

no movement in out of vein (salinity is same as body .9%

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30
Q

Hypertonic solution in veins

A

water moves into vein

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31
Q

Hypotonic solution in veins

A

water moves out of vein

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32
Q

Dependent Edema

A

edema on lowest part of the body.

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33
Q

Histamines cause capillaries to become ?

A

leaky.

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36
Q
Water Excess (clinical manifestations)
Hypervolemia
A
  • LOW blood through kidney
  • LOW cardiac output
  • Kidney disease
  • LOW Hematocrit
  • LOW Hemoglobin
  • LOW Serum Osmolality
  • UP Capillary permeability (histamines)
  • UP Capillary hystrostatic pressure
  • release ANP (fr atria) and BNP (fr ventricle)
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38
Q

SIADH

A

Syndrome of Inappropriate ADH

  • not making urine
  • fluid stays in vascul?
  • hypervolemic
  • UP Urine Specific Gravity
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39
Q

Diabetes Insipidus

A

not enough ADH

  • polyurea
  • LOW specific gravity
  • risk for dehydration
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40
Q

Vasopressin

A

aka ADH

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41
Q

Desmopressin

A

Synthetic version of Vasopressin

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42
Q

ANP(from atria) /BNP (from ventricle) released in response to ….

A

stretching of heart chambers. Tells kidney to release Na and water follows.

purpose: to INCREASE urine.

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43
Q

How and why ADH released?

A

Hypothalmus activated Pituitary Gland to secrete ADH in response to hypovolemia. Low BP

1) LOW BP - JGA releases Renin
2) in BLOOD: Renin becomes Angiotensin
3) in LIVER: Angiotensin I meets ACE (Angiotensin converting enzyme)

Angiotensin I becomes Angeiotensin II

Angiotensin II (potent vasoconstrictor, as circulates though body. everywhere it touches vasoconstricts.

4) Angiotensin II RAISES BP (patient still needs fluids though)
5) Angiotensin II stimulates Adrenal gland to release ALDOSTERONE.
6) Aldosterone tells kidneys to take Na out of GF so water follows (see diagram in notes)

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44
Q

ADH and Aldosterone raise BP by….

A

removing water from urine output

44
Q

Loop Diuretics do what?

A

ANP/BNP increase urine. As Na at loop of Henley attracting water creating more GF

45
Q

Anti HTN meds

A
  • Diuretics , get rid of fluids
  • ACE Inhibitors ( stops angiotensin I to II)
  • Direct vasodilator (open pipe so pressure goes down)

Symptoms: faint because veins dilated, low bp, not circulating well.

46
Q

Hyponatremia (LOW Na) symptoms

A
  • Hypervolemia?
  • 3Ds
  • burns
  • SIADH
  • too much too quick hypotonic fluid iv.

Nursing Implications

Muscle weakness
LOW HR and peristalsis rate
Potential Siezures
LOW temp

47
Q

Hypermatremia

A

CAUSES

  • Dehydration
  • diabetes insipidus
  • [ ] enteral fee
NURSING IMPLICATIONS
-muscle twitching
Thirst
Poor skin turgor
Dry sticky mucous membrane
Potential for edema
HTN (concentrated blood attracts water)
48
Q

HypoCalcemia

A

CAUSES
Post menopause
LOW vitD
Thyroid removal

NURS IMPLICATIONS

  • Tetany, twitches, carpal pedal spasms (truseaus)
  • Facial twitching (chvosteks sign)
  • Risk for fractures, pathological (just breaks from weakness, no trauma)
  • risk for osteoporosis

TREAT
Ca/VitD supplement

48
Q

HyperKalemia

A

CAUSE
dyrhytmia
Muscle spasms/cramps
Weakness

NURSE IMPLICATIONS

  • Kayexelate (binds K in gut)
  • Given as last resort to ESRD to have on hand in case of emergency, binds in gut causes diarrhea
48
Q

HypoKalemia

A

LOW K

CAUSES
3Ds
(Diuresis, Diarrhea, Diaphoresis)

NURSE IMPLICATIONS
dysrhythmia
Muscle weakness
Muscle cramps/spasms
LOW peristalsis
LOW vasodilation/constriction

TREAT
replace electrolytes (Gatorade)
K IV, dilute, very slow, NEVER push IV. NEVER IM
Used in lethal injection
K rich foods (bananas, dried fruit, citrus, peanuts, tomatoes)

48
Q

HypoMagnesemia

A

CAUSES
ETOH (alcohol abuse)
Malnourished
LOW GI absorption

NURSE IMPLICATIONS
Neuromuscular excitability
Seizures

TREAT

49
Q

HyperCalcemia

A

CAUSES
Immobility
UP serum because of leaching from bones
Multiple Myloma (bones hollow and snap)

NURSE IMPLICATIONS
Risk for Kidney stones
Lethargic
Muscle weakness/slow
Dysrhythia

TREAT

53
Q

HyperMagnesemia

A

CAUSES
Renal failure
Excess intake
Anyone who received Mg as a drug (mom?)

NURSIN IMPLICATIONS
Bradycardia
Respiratory Depression
Drug on hand (rescue med, Calcium Gluconate)

54
Q

Hypophosphatemia

A

CAUSES
Malnutrition
LOW gut absorption

NURSING IMPLICATIONS
Risk for infection
Risk for wounds
LOW healing

55
Q

Hyperphosphatemia

A

CAUSES
Renal failure

NURSING IMPLICATIONS

  • ESRD
  • Phosphate binder with all meals at same time as food.
  • if UP P, LOW Ca
  • LOW Ca = osteoclasts break down bone to put Ca back in serum

*** RENAL OSTEODYSTROPHY

56
Q

Phosphorous is in

A

All living things

57
Q

Insensible fluid loss

A

Evaporation from skin and lungs
Sweat
Breath

58
Q

Pressure inside artery is ?

A

Hydrostatic pressure
Filtration, water pushed out

(See pic)

60
Q

Percentage of interstitial fluid

Back in vein
Into Lymph

A

90 / 10

61
Q

Normal pH of body

A

7.35 - 7.45

62
Q

Acidosis starts at pH..

A

7.34 and BELOW
retention of CO2

(CO2 + H2O = H2CO3) carbonic acid

63
Q

Alkalosis starts at pH…

A

7.46 and UP

64
Q

Respiratory Acidosis

A

buildup of CO2

CAUSES/PATIENTS
-COPD:
Asthma (narrowing of airway)
Emphysema (alveolar lose elasticity, stretch balloon)
Chronic Bronchitis (mucus plugs)
-Hypo ventilation: stroke, opiates, Mg OD

RENAL COMPENSATION
retains bicarbonate (HCO3)
65
Q

what neutralizes Carbonic Acid

A

Carbonic Anhydrase

66
Q

Respiratory Alkalosis

A

loosing too much CO2

CAUSES/PATIENTS

  • Hyperventilation (hysterical person, crying baby, mom in labor)
  • Ventilator patients

TREATMENT
re-breath CO2, paper bag

67
Q

Metabolic Acidosis

A

CAUSES

  • Loss of pancreatic bicarbonate (loss of alkaline, you will become acidic)
  • Diabetic KetoAcidosis

BODY COMPENSATION

  • Kidneys retain bicarbonate
  • automatically body starts Kussmul Respiration (respiratory compensation) prolonged breathing to get rid of excess CO2
68
Q

Diabetic KetoAcidosis (what is happening)

A

see pic

  • if pancreas stops making insulin, cells die slowly.
  • cells become hungry because glucose in blood but no cells getting fed. the more the patient eats because the body said it’s hungry, the more glucose builds up in blood and doesn’t get to cells.

sugary blood attracts water causing

3Ps: Polyphagia (UP hunger), Polydypsia (UP thirst), Polyurea (UP urine)

69
Q

Gluconeogenesis

A

Gluconeogenesis (GNG) is a metabolic pathway that results in the generation of glucose from non-carbohydrate carbon substrates such as pyruvate, lactate, glycerol, and glucogenic amino acids. While primarily odd-chain fatty acids can be converted into glucose, it is possible for at least some even-chain fatty acids.

SEE PIC

TriGlycerides (fats)

GLYCEROL
FA FA FA

Glycerol used to make sugar from brain because glucose ingested not being used to feed cells. When body removes top glycerol from triglyceride, the remaining Fatty Acids become ketones making system acidic.

70
Q

Which way does fluid move (hypotonic, hypertonic)

A

from hypo - hyper tonic

71
Q

Hyperventilating (losing CO2) creates what pH?

A

alkaline

72
Q

Respiratory Acidosis common in pts w …

A

COPD

retaining too much CO2

73
Q

Long term COPD effects

A

LOW O2 becomes trigger to breath instead of acidosis in body. When body is acidic for so long, body gets used to it.

74
Q

In COPD pts, what setting for O2 flow rate?

A

2L/minute

75
Q

most common cause of Metabolic Acidosis

A

1) Diarrhea (loss of bicarbonate)
2) Diabetic KetoAcidosis (body uses glycerol to make glucose and leaves 3 Fatty Acids. Body does this because glucose in food is not being used to feed body and only sits in blood. (fruity breath)

76
Q

Body compensation for Metabolic Acidosis

A
  • Kidneys hold back bicarbonate to neutralize acid

- Kussmaul Respiration (prolonged exhale to get rid of excess CO2)

77
Q

Body compensation for Respiratory Acidosis

A
  • kidneys hold back bicarbonate.
  • body can’t fix respiratory problems with respiratory fix.
  • have to consciously teach pts pursed lip breathing.
78
Q

When P UP….then Ca

A

Ca LOW

-inverse relationship

79
Q

in ESRD pts, Hyperphosphotemia would be treated by giving what?

A

a P binder with every meal. Prevents P from reaching blood stream. Goes out with food.

80
Q

HypoCalcemia causes Renal….

A

Renal Osteodystrophy

inverse of Hyperphosphotemia

pituitary stimulates osteoclasts to release Ca from bones.

81
Q

Normal levels, K

A

3.5 - 5 meq/L

hypo: DOWN 3.5
hyper: UP 5

82
Q

Normal Levels, Na

A

135 - 145 meq/L

Hypo: DOWN 135 meq/L
Hyper: UP 145 meq/L

83
Q

ADH released from ?

A

Hypothalmus stimulates pituitary gland to secreet ADH.

84
Q

Diabetes insipidus has how much ADH?

A

not enough

polyurea
dilute urine

NURSE IMPLICATIONS
increase electrolytes
provide water because patient drinks alot
every 3 bottles water, 1 bottle gatorade

85
Q

Adenoma

A

Gland/Tumor

can secrete ADH

86
Q

Who takes ACE inhibitors

A

The body reacts to slight drops in BP for some people by starting RAAS process. Not necessary, so these patients take ACE inhibitors to prevent it.

87
Q

RAAS system stimulated by?

A

Low BP
Sudden Shock
(loss of limb/blood) or
Anaphalactic Shock (fluid shift out of blood into interstitial fluid, possible from leaky capillaries due to histamine)

88
Q

Most fluid in the body is in which cells?

A

1st) Intra cellular

2) Extra cellular (blood, interstitial)

89
Q

1L fluid = ? lbs

1L fluid = ? KILO

A

1L fluid = 2.2 lbs

1L fluid = 1 Kilo

90
Q

1oz = 30ml

A
1TB = 15ml
2TB = 1oz
1tsp = 5ml
91
Q

When taking Daily Weigh, what should be the same

A

same scale
same time
same clothes

92
Q

Normal Urine output

A

30cc/hour

15cc (renal insufficiency, not enough to clear out waste)

93
Q

Metabolic Alkalosis (7.46UP)

A

Vomiting
Secution (gastric)
too much proton pump inhibitor

94
Q

Allen’s Test

A

press down on both ulnar and radial artery (wrist), then release ulnar, keeping pressure on radial. If blood flows back in, there is no blockage and the radial artery can be stuck. (injection)

95
Q

ABG

A

Arterial Blood Gas test

96
Q

Amount of Calories?

Protein, Carb, Fat

A
Protein = 4 cal
Carb = 4 cal
Fat = 9 cal
97
Q

Normal Na ingested per day

A

500mg

98
Q

Fat or Water soluble?

Vit A, D, E, K

A

Fat

99
Q

Normal Fluid intake

A

2500ml

100
Q

Third Spacing

A

shift of fluid from vascular space into are where not available to support normal physiologic processes.

100
Q

Main cause of fluid excess

A

HyperNatremia

101
Q
normal    pH = 7.35 - 7.45
normal    pCO2 = 35 - 45 (retain CO2, UP Acid)
                (respiratory)
normal    HCO3 = 22 - 26 (Bi-carb) 
                (metabolic)
A

ACID ——————ALKALINE

pH 7.35 - 7.45

102
Q

CO2 + H2O =

A

HCO3

Carbonic Acid