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NSCC 7520 Critical Care Theory 4 > Fluid & Electrolytes + Liver > Flashcards

Fluid & Electrolytes + Liver Flashcards

1
Q

define osmolality

A

solute particles per Kg of solvent

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2
Q

define osmolarity

A

solute particles per L of solvent

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3
Q

What is the distribution of fluid in the body

A

1/3 extracellular

2/3 intracellular

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4
Q

What ions are intracellular

A

K+
Mg2+
HPO4-
Proteins

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5
Q

what ions are extracellular

A

Na+
HCO3-
Cl-
Ca+

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6
Q

What is extracellular fluid divided into

A

1/3 vascular

2/3 interstitial

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7
Q

What are the 3 forces that regulate fluid movmement

A

osmosis
hydrostatic pressure
oncotic pressure

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8
Q

define osmosis

A

movement of H20 from an area of high concentration to an area of low concentration

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9
Q

define hydrostatic pressure

A

force of the blood as it pushes on the capillary walls

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10
Q

T or F hydrostatic pushes small proteins out of the capillaries into the interstitial space

A

T

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11
Q

define oncotic pressure

A

pulls fluid from the surrounding tissues back into the capillaries

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12
Q

What drives filtration

A

hydrostatic fluid

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13
Q

what drives reabsorption

A

oncotic fluid

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14
Q

what are the two forces that regulate solute movmemnt

A

diffusion

active transport

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15
Q

what is diffusion

A

movement of solute particles from an area of high concentration to low concentration

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16
Q

Is energy required for diffusion

A

no

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17
Q

What is active transport

A

solutes moving against contentration gradient
from [low] to [high]
requires ATP

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18
Q

What 3 things play a part in production of ATP and proper fn of the sodium/potassium pump

A

magnesium
phosphate
thiamine

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19
Q

What is ADH

A

antidiuretic hormone aka vasopressin

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20
Q

how does ADH work

A

stimulates water reabsorption
opens small channels in collecting duct
water moves through these channels from [low] (collecting duct) to [high] (blood)

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21
Q

What is ADH release triggered by

A

osmotic sensors
baroreceptors
RAA system

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22
Q

Where are the osmotic sensors that trigger ADH release? how do they work

A

hypothalamus

reacts to the concentration of solutes in your blood

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23
Q

Where are the baroreceptors that trigger ADH release? how do they work?

A

Lt atrium, carotid artery and aortic arch –> react to decreased arterial pressure

rt atrium and vena cavas react to less volume returning to the heart

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24
Q

What organ is essential in regulating fluid volume

A

kidneys

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25
Q

what triggers the RAA system (3)

A

decreased BP in the glomerulus
SNS stimulation of the kidneys
decrease in Na+ concentration in the distal tubule

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26
Q

How is angiotensin 2 released

A

kidneys secrete renin
angiotensinogen from liver converts renin to angiotensin 1
ACE from the lungs converts angiotensin 1 to angiotensin 2

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27
Q

what does angiotensin 2 do? What does this mean for preload and afterload?

A

arterial vasoconstrictor (inc afterload)

stimulates ADH from posterior pituitary (inc preload and afterload (vasopressin))

stimulates aldosterone release (inc preload)

stimulates SNS activity (inc preload, afterload and contractility)

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28
Q

Where is aldosterone produced

A

adrenal cortex

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29
Q

What does aldosterone do

A

triggers reabsorption of Na+ (and H20) from nephron collecting duct back to bloodstream

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30
Q

is aldosterone reabsorption passive?

A

no, active transport requires ATP

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31
Q

What ion does aldosterone cause to be excreted in urine

A

K+

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32
Q

Which hormone causes the movement of both fluids and solutes

A

aldosterone

Sodium and water

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33
Q

What is aldosterone release triggered by (2)

A

stress response of the hypothalamus

RAA system

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34
Q

what are two stress hormones

A

cortisol

aldosterone

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35
Q

where do thiazide diuretics work

A

distal tubule

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36
Q

what are 2 examples of thiazide diuretics

A

HCTZ

metolazone

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37
Q

Where do loop diuretics work

A

ascending portion of the loop of Henle and distal renal tubule

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38
Q

What is an example of a loop diuretic

A

lasix

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39
Q

what do both thiazide and loop diuretics do

A

decrease Na+ & Cl- reabsorption - loss of Na+ & H20

also causes hypokalemia

loss of hydrogen ions

chloride is excreted/bicarb is retained

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40
Q

What type of relationship do chloride and bicarb have

A

inverse

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41
Q

what acid-base imbalance can diuretics cause? why? what type of diuretic more commonly causes this?

A

metabolic alkalosis

cause chloride to be excreted and since bicarb has an inverse relationship with chloride it is retained

loop diuretics

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42
Q

What type of diuretics cause loss of bicarb, sodium, ater and potassium

A

carbonic anhydrase inhibitors (acetazolamide)

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43
Q

how do potassium sparing diuretics work? what is an example of one?

A

inhibits aldosterone - decreased sodium reabsorption thereby preventing potassium secretion

spironolactone

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44
Q

what can spironolactone cause

A

hyperkalemia

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45
Q

What peptides are released in response to myocardial stretch? what do they cause?

A

ANP & BNP

vasodilation
loss of Na+ & H20
inhibits the SNS and RAA

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46
Q

What do ANP AND BNP result in

A

increased urine output
decreased blood volume - decreased preload
does not impact osmolality

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47
Q

What do ANP and BNP affect solute and solvent

A

move both fluids and solutes in proportion to each other

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48
Q

What triggers ANP release? where is it secreted?

A

mainly secreted in atrium

triggered by hypernatremia and myocardial stretch

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49
Q

where is BNP secreted? How is BNP release triggered?

A

secreted by the ventricles

triggered by myocardial stretch

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50
Q

What is tonicity

A

ability of a solution to make water move in and out of cells

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51
Q

What are the three different types of fluid

A

isotonic - same osmolality btw plasma and cells
hypotonic - lower osmolality in plasma then cells
hypertonic - higher osmolality in plasma then cells

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52
Q

what is the term for balanced/normal amt of fluid volume

A

euvolemic

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53
Q

what is the term given for too much fluid volume

A

hypervolemic

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54
Q

what is the term given for too little fluid volume

A

hypovolemic

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55
Q

What is the term for ratio of RBC to total volume of blood in a sample

A

hematocrit

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56
Q

What can hematocrit tell us

A

is an indicator of concentration - good for trending

low Hct = more dilute
high hct = more concentrated

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57
Q

In acidosis what happens in the blood regarding hydrogen and potassium

A

there are too many hydrogen ions in the blood so hydrogen begins to move into the cells and potassium moves out

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58
Q

what happens with hydrogen and potassium in alkalosis

A

not enough hydrogen ions in the blood so hydrogen moves out

potassium moves in

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59
Q

what hormone is responsible for telling cells to take in glucose

A

insulin

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60
Q

when moves into the cell with glucose

A

potassium

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61
Q

What is required to move potassium into a cell

A

magnesium, thiamine and phosphate to operate K+/Na+ pump

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62
Q

what moves out of a cell as glucose and potassium move in

A

Na+

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63
Q

How many forms of serum calcium are there? what are they?

A

2

ionized & bound

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64
Q

what is the difference between ionized calcium and bound calcium

A

ionized calcium - free/active

bound - bound mostly to albumin but some other proteins

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65
Q

which one of the calcium forms is most responsible for calcium related functions

A

ionized

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66
Q

What do calcium and hydrogen compete for binding sites on

A

albumin

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67
Q

What happens to calcium in acidosis

A

greater number of hydrogen ions competing with calcium for binding sites on albumin

the amount of bound calcium falls and ionized calcium goes up

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68
Q

What happens to bound calcium and ionized calcium in acidosis? alkalosis?

A

acidosis: bound goes down, ionized up to compete with H+ ions
alkalosis: bound goes up, ionized go down

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69
Q

what should you consider when replacing albumin

A

ionized calcium level

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70
Q

what are 3 causes of metabolic acidosis

A

lactic acidosis
renal dysfunction
loss of bicarbonate

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71
Q

Below what acidotic pH level do we begin to get concerned? why?

A

7.2

vasoactive drugs do not work as well

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72
Q

What is a primary electrolyte in the extracellular fluid

A

sodium

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73
Q

what is the normal range for sodium

A

135-145

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74
Q

What are the 4 main functions of Na+

A

ECF osmolality/tonicity
fluid balance
cellular depolarization - part of action potential

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75
Q

What are the 3 ways in which Na+ is regulated

A

retained or excreted by kidneys
influenced by aldosterone and ANP
moved by Na+/k+ pump

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76
Q

What is the cardinal rule for Na+

A

always followed by water

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77
Q

What are the two main causes of hyponatremia? what is the main one

A

dilutional (main)

low intake

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78
Q

what are three things that can cause dilutional hyponatremia

A

heart failure
SIADH
excess free H2O

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79
Q

What are 4 clinical manifestations of hyponatremia

A

H2O moves into cell causing them to lyse

CNS effects - confusion, irritability, seizures

low serum osmolality

HA, muscle weakness

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80
Q

below what sodium level do you see seizures and delirium

A

Na+ <110

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81
Q

how do you treat hyponatremia

A

fluid restriction
increase H2O
administer hypertonic NaCl (3%)

82
Q

What are 2 causes of hypernatremia

A

water deficit

loss of hypotonic solutes

  • diarrhea
  • GI losses
  • diuresis
  • DI
83
Q

What are clinical manifestations of hypernatremia (5)

A

cells shrivel as H20 moves out

CNS symptoms - twitching, seizures, coma

thirst

high serum osmolality

fever, flushed skin

84
Q

What is the treatment for hypernatremia

A

slowly replace H20 as needed with IV D5W or free water in enteral feeds

limit Na+ intake

treat underlying cause

85
Q

What is the primary electrolyte in intracellular fluid

A

K+

86
Q

what is the normal range for K+? what about in cardiac?

A

3.5-5

4-5

87
Q

What are the 3 functions of K+

A

essential for nerve impulse conduction
muscle contraction

acid/base balance

ICF osmolality

88
Q

How is potassium regulated

A

balance in body mainly controlled by dietary intake and kidneys

Na+/K+ pump and diffusion

influenced by acid-base balance: H+ and K+ move in and out of cells opposite of each other in response to serum pH changse

89
Q

What are 4 causes of Hypokalemia

A

inadequate intake

GI losses

Diuresis

Shift into cells due to alkalosis or movement of glucose/insulin

90
Q

What are 3 clinical manifestations of hypokalemia

A

flattened T waves

dysrhythmias

skeletal muscle weakness

91
Q

How do you treat hypokalemia (4)

A

replacement of lost (as opposed to displaced) K-

correction of acid-base balance

ensure adequate nutrition

reconsider meds such as diuretics that are contributing to loss

92
Q

What are 4 causes of hyperkalemia

A

high intake

renal dysfunction

shifts out of cells d/t acidosis

cell injury/death release K+

93
Q

what are 4 manifestations of hyperkalemia

A

ECG changes - peaked T waves

bradycardia and blocks

skeletal muscle weakness

cramps, nausea

94
Q

Treatment for hyperkalemia

A

resolve acid/base imbalance

promote removal with diuretics

K-binding resins (kayexalate)

dialysis

stabilize cell membrane by ensuring adequate Ca2+

shift by administering d50 followed by insulin

95
Q

What is the distribution of phosphate

A

80% found in bones

20% in ICF (tiny bit in ECF)

96
Q

what is the normal range for phosphate

A

0.9-1.4

97
Q

What are the 3 functions of phosphate

A

cell membrane structure

FORMATION OF ATP AND 2,3 DPG WHICH IS USED IN BINDING OF O2 TO HGB

co-factor in intracellular enzyme reactions

98
Q

where is phosphate absorbed

A

GI tract

99
Q

what does phosphate compete with for absorption

A

Ca2+

100
Q

What type of relationship do PO4 and Ca2+ have? what are they regulated by

A

inverse relationship - regulated by the parathyroid hormone

101
Q

What happens to phosphate when calcium increases

A

decreases

102
Q

which acid/base balance problem causes phosphate to move into cells

A

alkalosis

103
Q

when insulin moves glucose into the cells what goes in with it

A

K+

PO4-

104
Q

what are 3 causes of hypercalcemia

A

cancer, especially bone mets

renal dysfunction Ca2+ is excreted by the kidneys

hyperparathyroidism (increases Ca2+ release from bones and increases absorption)

105
Q

What are 4 clinical manifestations for hypercalcemia

A

decreased cell membrane excitability

CNS: fatigue, confusion, depression

Neuromuscular: muscle weakness, hyporeflexia

CVS: dysrhythmias, shortened QT, short ST

106
Q

What is the treatment for hypercalcemia (5)

A

correct PO4 levels (inverse relationship)

ensure adequate fluid volume to support urine output

correct acid-base imbalances

diuretics

dialysis

107
Q

What is the normal range for chloride

A

100-112 mmol/L

108
Q

what are 2 functions for chloride

A

along with Na+ helps regulate serum osmolality

helps maintain acid/base balance

109
Q

what are 3 ways chloride is regulated

A

ingested (NaCl)

reabsorbed or excreted by the kidneys as required to maintain acid/base balance

inverse relationship with bicarbonate HCO3-

110
Q

what does chloride have an inverse relationship with

A

bicarbonate

111
Q

What are some causes of hypochloremia (4)

A

sodium deficit

excess HCO3-

GI losses - vomiting/suctioning/diarrhea

increased renal losses (diuretics)

112
Q

what are clinical manifestations of hypochloremia in CNS

A

overexcitability

cramps, twitching, agitation

seizures, coma (severe)

113
Q

what can hypochloremia cause in CVS

A

dysrhythmias

114
Q

what acid/base imbalance makes us concerned about hypochloremia

A

alkalosis including low Na+ or K+

115
Q

what is the treatment for hypochloremia

A

correct underlying cause such as acid/base imbalance

ensure adequate hydrationm

116
Q

what are 3 causes of hyperchloremia

A

sodium excess (large and rapid infusions of NS)

bicarbonate deficit

acidosis

117
Q

what are 4 clinical manifestations of hyperchloremia

A

signs of metabolic acidosis (tachypnea, lethargy, weakness)

dysrhythmias, decreased CO

decreased LOC/coma

role in acid/base balance will also affect Na+ and K+ levels

118
Q

what is normal osmolarity of plasma

A

290 mOsm/L

119
Q

where is hydrostatic pressure the greatest

A

arterial end of capillary system

aortas

120
Q

where can hydrostatic pressure build up and cause problems

A

pulmonary vascular system –> fluid backs up into pulmonary system causing pulmonary edema

121
Q

where in the vascular system is oncotic pressure the greatest

A

venous end of capillary system

122
Q

what solute in our blood is most responsible for maintaining oncotic pressure

A

albumin

123
Q

where is the best example of diffusion in the body

A

gas exchange in the lungs

124
Q

how does the sodium-potassium pump work

A

active transport

125
Q

what does the Na+/K+ pump need to work

A

ATP!

126
Q

which hormone causes just water to be reabsorbed back into the bloodstream from the nephrons collecting duct

A

ADH

127
Q

which hormones are released as a consequence of the RAA system

A

aldosterone and ADH

128
Q

what hormone in the collecting ducts in the nephron to retain sodium and water and excrete potassium

A

aldosterone

129
Q

what does adding fluid to a solution do to its concentration

A

decrease its osmolarity

130
Q

prior to intervention, a rapidly bleeding patient is experiencing which of the following

A

isotonic hypovolemia

131
Q

what would a rapidly bleeding patients hematocrit be

A

normal

132
Q

you administered lasix and your patient produces 2L of fluid in the following 3 hours. what changes would you expect to see in their hematocrit

A

increased hematocrit

133
Q

what state would a patient who was over-rescuitated with plasmalyte and NS be experiencing

A

isotonic hypervolemia

134
Q

what state can SIADH cause

A

hypotonic hypervolemia

135
Q

an elderly person with communication challenges in long term care is at risk for experiencing what state

A

hypertonic hypovolemia

136
Q

which volume and concentration state is induced to treat cerebral vasospasm

A

isotonic hypervolemia

137
Q

what medication is given for cerebral vasospasm

A

nimlodopine Ca2+ channel blocker that works on smooth muscle

138
Q

what happens when you have blood in the brain regarding CSF

A

blocks reuptake causing hydrocephalus

139
Q

receives blood flow from how many sources

A

2
25% hepatic artery - directly from the blood
75% - portal vein nutrient rich blood from gut, stomach, spleen and pancreas is oxygen poor

140
Q

what two organs dont go through the liver

A

legs and kidneys

141
Q

does blood flow through liver in capillaries

A

no sinusoids

142
Q

what are the major functional cells of the liver

A

hepatocyte

143
Q

what liver cells conjugate bilirubin

A

hepatocytes

144
Q

what do hepatocytes do

A

perform metabolic, secretory and ednocrine fn

conjugate bilirubin

145
Q

what cells make up 70% of bodies macrophages

A

Kupffer cells in liver

146
Q

What do Kupffer cells do

A

make up 70% of bodies macrophages
produce cytokines (triggered by endotoxins)
filter bacteria and endotoxins
destroy worn RBC, WBC, and bactera

147
Q

where are kupffer cells found

A

in the lining of the sinusoids of the liver

148
Q

what are 6 fn of the liver

A

carbohydrate, protein and lipid metabolism

synthesis of clotting factors

bile production

filtration of “old” red blood cells

storage of vitamins and minerals

detoxification, bacteria removal and cell clean-up

149
Q

What are 3 processes of carbohydrate metabolism in the liver

A

glycogenesis - converts glucose to glycogen

glycogenolysis - breaks down glycogen back to glucose

gluconeogeneis - converting non-carbohydrate things such as amino acids and proteins into glucose

150
Q

what does the liver do with amino acids

A

converts them to glucose or lipids

151
Q

What organ syntehsizes amino acids

A

liver

152
Q

what 3 plasma protein are formed in the liver

A 
albumin (60^ of plasma proteins)
globulins (immune function)
clotting factors (fibrinogen, prothrombin and factors V, VII, IX and X)
153
Q

what hormone does the liver inactivate

A

GROWTH HORMONE

154
Q

What blood vessel does blood flow out of the liver

A

hepatic vein

155
Q

what does the liver do with excess carbs and proteins

A

converts them into fatty acid and triglycerides which are sent out for storage in adipose tissue

156
Q

What does the liver create cholesterol out of

A

fatty acids

157
Q

what does the liver do with trigylcerides

A

oxidizes them to produce energy

158
Q

what happens in gluconeogenesis

A

fats are converted to glycogen and stored for energy

159
Q

The liver stores what vimtamins

A

A, D, E and K (fat soluble)

vitamin B12

160
Q

what minerals are stored in the liver

A

iron and copper

161
Q

Where does the body store a back up supply of blood

A

in the sinusoids of the liver

162
Q

what hormones does the liver inactivate (6_

A

aldosterone, cortisol, epinephrine

growth hormone, glucagon, glucocorticoids

163
Q

what do kupffer cells do

A

detoxification of drugs and toxins

removes bacteria, antigens and byproducts of coagulation

164
Q

Where in the body is lactate cleared

A

liver

165
Q

what creates ammonia

A

created in the gut and cells during the breakdown of protein

166
Q

How is ammonia removed from the body

A

the liver converts ammonia to water soluble urea

167
Q

4 ways in which the liver can be acutely injured

A

Tylenol OD
shock states
viral infection
budd chiari syndrome

168
Q

what are two chronic causes of liver injury

A

EtOH and non alcohol liver disease

chronic viral hepatitis (B, C)

169
Q

why does liver failure cause decreased LOC

A

unable to convert ammonia to H20 soluble urea which crosses BBB affecting astroctyes causing creation of osmotically active substances causing cerebral edema

accumulation of medications and their metabolites

170
Q

why does liver failure cause bleeding

A

unable to creat clotting factors

portal HTN causes the formation of variceis

unable to store vitamin K

171
Q

why does liver failure cause edema,a sites, leaking wound sites

A

unable to create albumin causing decreased oncotic pressure (unable to pull fluid)

backflow of blood from damaged liver

172
Q

why does liver failure cause jaundice

A

unable to conjugate bilirubin and excrete it so you have excess bilirubin

173
Q

why does liver failure lead to increased chance of infection

A

unable to produce globulins which are important in immune function

unable to produce cytokines

poor nutrition

large portion of marcophages are found in the liver

bacteria can pass through a damaged liver without being broken down

174
Q

why does portal HTN occur in liver failure

A

liver becomes cirrhosed and blood is unable to flow through it

175
Q

why does hypoglycemia occur in liver failure

A

unable to perform glycogenolysis and gluconeogenesis

impaired carbohydrate metabolism

176
Q

What are LFTs

A

AST, ALT, Albumin, PT/INR, alk phos, GGT, bilirubin, ammonia, platelets

177
Q

What is AST? where is it found? is it specific for the liver?

A

asparate aminotransferase
found in the liver, heart, skeletal muscle, pancrease and kidneys

low specificity to the liver

178
Q

What enzyme found in hepatocytes is most specific to the liver

A

ALT

179
Q

Does decreasing ALT/AST mean that your pts liver is improving

A

not necessarily, could mean that your pateints liver injury has progressed to the point they have few functioning hepatocytes

180
Q

What does albumin tell us

A

chronic liver failure indicator as albumin has a long half life of 20 days

181
Q

what is a good indicator of chronic liver injury

A

albumin

182
Q

is albumin specific

A

no a decrease could be liver, could be leaking out such as sepsis or trauma or could be malnourished

183
Q

What is a very sensitive indicator of liver dysfunction that is often the first to be affected

A

PTT and INR since the liver synthesizes so many clotting factors

184
Q

is alk phos able to tell us liver function on its own?

A

no need GGT as well

185
Q

what is alk phos? where is it commonly found?

what is is most specific for on its own

A

alkaline phosphatase
found in may tissues mostly bone and liver
most specific for bone disease

186
Q

what is GGT? what does it do? where is it found? Where is it most concentrated?

A

gammaglutamyl transferase

assists amino acids across membranes

liver, kidney, pancreas, heart and brain
most concetnrated in biliary ductules that carry bile to the bile ducts so very sensitvie but non specific indicator or hepatobiliary disease

187
Q

if you have a high alk phos and GGT what does this mean

A

liver porblem

188
Q

if you have a high alk phos and normal ggt what does this mean

A

bone problem

189
Q

Why do we check platelet levels in our LFTs

A

liver produces thrombopoietin which tells the bone marrow to increase platelet production

190
Q

What is refeeding syndrome

A

potential fatal shift in fluid and electrolytes that occurs when re-introducing malnourished patients to any form of nutrition

191
Q

what time frame does re-feeding syndrome occur in

A

12-72 hours after refeeding is initaited

192
Q

how long can refeeding syndrome continue for

A

2-7 days

193
Q

what are three things that occur during times of malnourishment

A

body maintains glucose levels from glycogen stores (about a days worth)

then switches to gluconeogenesis which uses fats and amino acids from protein catabolism for energy

intracellular electrolytes (K, Mg, and PO4) and calcium from the bones are depleted from within the cells

water, vitamin and mineral depletion occurs as well

194
Q

what occurs when we start refeeding malnourished patients

A

carbs are used for metabolism
blood glucose increases
insulin released
moves glucose, K+, PO4- into cells using thiamine
sodium potassium pump kicks in and uses magnesium
sodium moves out of the cell d/t Na+/K+ pump which leads to edema and fluid overload

195
Q

what specifically causes edema to occur in refeeding syndrome

A

sodium moving out of the cell as K+ moves in

196
Q

what is the main electrolyte imbalance that is a hallmark sign of refeeding syndrome

A

hypophosphatasemia

197
Q

What are 5 signs of refeeding syndrome

A 
hypophosphatemia 
abnormalities in fluid balance
vitamin deficiency e.g. vitamin B1 (thiamine)
hypomagnesaemia
hypokalemia
198
Q

what can the electrolyte and fluid balance abnormalities in refeeding syndrome cause

A

cardiac, respiratory and neuromuscular consequences

199
Q

how do we start feeding pts suspected of refeeding syndrome

A

slowly

200
Q

what should we monitor for refeeding syndrome

A

blood work closely and replacement of electrolytes

201
Q

What is thiamine absolutely necessary for

A

ATP

202
Q

what are three things that occur with low thiamine

A

muscle weakness
Wernicke syndrome
HF

NSCC 7520 Critical Care Theory 4 (5 decks)

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