Fluid & Electrolytes + Liver Flashcards
define osmolality
solute particles per Kg of solvent
define osmolarity
solute particles per L of solvent
What is the distribution of fluid in the body
1/3 extracellular
2/3 intracellular
What ions are intracellular
K+
Mg2+
HPO4-
Proteins
what ions are extracellular
Na+
HCO3-
Cl-
Ca+
What is extracellular fluid divided into
1/3 vascular
2/3 interstitial
What are the 3 forces that regulate fluid movmement
osmosis
hydrostatic pressure
oncotic pressure
define osmosis
movement of H20 from an area of high concentration to an area of low concentration
define hydrostatic pressure
force of the blood as it pushes on the capillary walls
T or F hydrostatic pushes small proteins out of the capillaries into the interstitial space
T
define oncotic pressure
pulls fluid from the surrounding tissues back into the capillaries
What drives filtration
hydrostatic fluid
what drives reabsorption
oncotic fluid
what are the two forces that regulate solute movmemnt
diffusion
active transport
what is diffusion
movement of solute particles from an area of high concentration to low concentration
Is energy required for diffusion
no
What is active transport
solutes moving against contentration gradient
from [low] to [high]
requires ATP
What 3 things play a part in production of ATP and proper fn of the sodium/potassium pump
magnesium
phosphate
thiamine
What is ADH
antidiuretic hormone aka vasopressin
how does ADH work
stimulates water reabsorption
opens small channels in collecting duct
water moves through these channels from [low] (collecting duct) to [high] (blood)
What is ADH release triggered by
osmotic sensors
baroreceptors
RAA system
Where are the osmotic sensors that trigger ADH release? how do they work
hypothalamus
reacts to the concentration of solutes in your blood
Where are the baroreceptors that trigger ADH release? how do they work?
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
What organ is essential in regulating fluid volume
kidneys
what triggers the RAA system (3)
decreased BP in the glomerulus
SNS stimulation of the kidneys
decrease in Na+ concentration in the distal tubule
How is angiotensin 2 released
kidneys secrete renin
angiotensinogen from liver converts renin to angiotensin 1
ACE from the lungs converts angiotensin 1 to angiotensin 2
what does angiotensin 2 do? What does this mean for preload and afterload?
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)
Where is aldosterone produced
adrenal cortex
What does aldosterone do
triggers reabsorption of Na+ (and H20) from nephron collecting duct back to bloodstream
is aldosterone reabsorption passive?
no, active transport requires ATP
What ion does aldosterone cause to be excreted in urine
K+
Which hormone causes the movement of both fluids and solutes
aldosterone
Sodium and water
What is aldosterone release triggered by (2)
stress response of the hypothalamus
RAA system
what are two stress hormones
cortisol
aldosterone
where do thiazide diuretics work
distal tubule
what are 2 examples of thiazide diuretics
HCTZ
metolazone
Where do loop diuretics work
ascending portion of the loop of Henle and distal renal tubule
What is an example of a loop diuretic
lasix
what do both thiazide and loop diuretics do
decrease Na+ & Cl- reabsorption - loss of Na+ & H20
also causes hypokalemia
loss of hydrogen ions
chloride is excreted/bicarb is retained
What type of relationship do chloride and bicarb have
inverse
what acid-base imbalance can diuretics cause? why? what type of diuretic more commonly causes this?
metabolic alkalosis
cause chloride to be excreted and since bicarb has an inverse relationship with chloride it is retained
loop diuretics
What type of diuretics cause loss of bicarb, sodium, ater and potassium
carbonic anhydrase inhibitors (acetazolamide)
how do potassium sparing diuretics work? what is an example of one?
inhibits aldosterone - decreased sodium reabsorption thereby preventing potassium secretion
spironolactone
what can spironolactone cause
hyperkalemia
What peptides are released in response to myocardial stretch? what do they cause?
ANP & BNP
vasodilation
loss of Na+ & H20
inhibits the SNS and RAA
What do ANP AND BNP result in
increased urine output
decreased blood volume - decreased preload
does not impact osmolality
What do ANP and BNP affect solute and solvent
move both fluids and solutes in proportion to each other
What triggers ANP release? where is it secreted?
mainly secreted in atrium
triggered by hypernatremia and myocardial stretch
where is BNP secreted? How is BNP release triggered?
secreted by the ventricles
triggered by myocardial stretch
What is tonicity
ability of a solution to make water move in and out of cells
What are the three different types of fluid
isotonic - same osmolality btw plasma and cells
hypotonic - lower osmolality in plasma then cells
hypertonic - higher osmolality in plasma then cells
what is the term for balanced/normal amt of fluid volume
euvolemic
what is the term given for too much fluid volume
hypervolemic
what is the term given for too little fluid volume
hypovolemic
What is the term for ratio of RBC to total volume of blood in a sample
hematocrit
What can hematocrit tell us
is an indicator of concentration - good for trending
low Hct = more dilute
high hct = more concentrated
In acidosis what happens in the blood regarding hydrogen and potassium
there are too many hydrogen ions in the blood so hydrogen begins to move into the cells and potassium moves out
what happens with hydrogen and potassium in alkalosis
not enough hydrogen ions in the blood so hydrogen moves out
potassium moves in
what hormone is responsible for telling cells to take in glucose
insulin
when moves into the cell with glucose
potassium
What is required to move potassium into a cell
magnesium, thiamine and phosphate to operate K+/Na+ pump
what moves out of a cell as glucose and potassium move in
Na+
How many forms of serum calcium are there? what are they?
2
ionized & bound
what is the difference between ionized calcium and bound calcium
ionized calcium - free/active
bound - bound mostly to albumin but some other proteins
which one of the calcium forms is most responsible for calcium related functions
ionized
What do calcium and hydrogen compete for binding sites on
albumin
What happens to calcium in acidosis
greater number of hydrogen ions competing with calcium for binding sites on albumin
the amount of bound calcium falls and ionized calcium goes up
What happens to bound calcium and ionized calcium in acidosis? alkalosis?
acidosis: bound goes down, ionized up to compete with H+ ions
alkalosis: bound goes up, ionized go down
what should you consider when replacing albumin
ionized calcium level
what are 3 causes of metabolic acidosis
lactic acidosis
renal dysfunction
loss of bicarbonate
Below what acidotic pH level do we begin to get concerned? why?
7.2
vasoactive drugs do not work as well
What is a primary electrolyte in the extracellular fluid
sodium
what is the normal range for sodium
135-145
What are the 4 main functions of Na+
ECF osmolality/tonicity
fluid balance
cellular depolarization - part of action potential
What are the 3 ways in which Na+ is regulated
retained or excreted by kidneys
influenced by aldosterone and ANP
moved by Na+/k+ pump
What is the cardinal rule for Na+
always followed by water
What are the two main causes of hyponatremia? what is the main one
dilutional (main)
low intake
what are three things that can cause dilutional hyponatremia
heart failure
SIADH
excess free H2O
What are 4 clinical manifestations of hyponatremia
H2O moves into cell causing them to lyse
CNS effects - confusion, irritability, seizures
low serum osmolality
HA, muscle weakness
below what sodium level do you see seizures and delirium
Na+ <110
how do you treat hyponatremia
fluid restriction
increase H2O
administer hypertonic NaCl (3%)
What are 2 causes of hypernatremia
water deficit
loss of hypotonic solutes
- diarrhea
- GI losses
- diuresis
- DI
What are clinical manifestations of hypernatremia (5)
cells shrivel as H20 moves out
CNS symptoms - twitching, seizures, coma
thirst
high serum osmolality
fever, flushed skin
What is the treatment for hypernatremia
slowly replace H20 as needed with IV D5W or free water in enteral feeds
limit Na+ intake
treat underlying cause
What is the primary electrolyte in intracellular fluid
K+
what is the normal range for K+? what about in cardiac?
3.5-5
4-5
What are the 3 functions of K+
essential for nerve impulse conduction
muscle contraction
acid/base balance
ICF osmolality
How is potassium regulated
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
What are 4 causes of Hypokalemia
inadequate intake
GI losses
Diuresis
Shift into cells due to alkalosis or movement of glucose/insulin
What are 3 clinical manifestations of hypokalemia
flattened T waves
dysrhythmias
skeletal muscle weakness
How do you treat hypokalemia (4)
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
What are 4 causes of hyperkalemia
high intake
renal dysfunction
shifts out of cells d/t acidosis
cell injury/death release K+
what are 4 manifestations of hyperkalemia
ECG changes - peaked T waves
bradycardia and blocks
skeletal muscle weakness
cramps, nausea
Treatment for hyperkalemia
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
What is the distribution of phosphate
80% found in bones
20% in ICF (tiny bit in ECF)
what is the normal range for phosphate
0.9-1.4
What are the 3 functions of phosphate
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
where is phosphate absorbed
GI tract
what does phosphate compete with for absorption
Ca2+
What type of relationship do PO4 and Ca2+ have? what are they regulated by
inverse relationship - regulated by the parathyroid hormone
What happens to phosphate when calcium increases
decreases
which acid/base balance problem causes phosphate to move into cells
alkalosis
when insulin moves glucose into the cells what goes in with it
K+
PO4-
what are 3 causes of hypercalcemia
cancer, especially bone mets
renal dysfunction Ca2+ is excreted by the kidneys
hyperparathyroidism (increases Ca2+ release from bones and increases absorption)
What are 4 clinical manifestations for hypercalcemia
decreased cell membrane excitability
CNS: fatigue, confusion, depression
Neuromuscular: muscle weakness, hyporeflexia
CVS: dysrhythmias, shortened QT, short ST
What is the treatment for hypercalcemia (5)
correct PO4 levels (inverse relationship)
ensure adequate fluid volume to support urine output
correct acid-base imbalances
diuretics
dialysis
What is the normal range for chloride
100-112 mmol/L
what are 2 functions for chloride
along with Na+ helps regulate serum osmolality
helps maintain acid/base balance
what are 3 ways chloride is regulated
ingested (NaCl)
reabsorbed or excreted by the kidneys as required to maintain acid/base balance
inverse relationship with bicarbonate HCO3-
what does chloride have an inverse relationship with
bicarbonate
What are some causes of hypochloremia (4)
sodium deficit
excess HCO3-
GI losses - vomiting/suctioning/diarrhea
increased renal losses (diuretics)
what are clinical manifestations of hypochloremia in CNS
overexcitability
cramps, twitching, agitation
seizures, coma (severe)
what can hypochloremia cause in CVS
dysrhythmias
what acid/base imbalance makes us concerned about hypochloremia
alkalosis including low Na+ or K+
what is the treatment for hypochloremia
correct underlying cause such as acid/base imbalance
ensure adequate hydrationm
what are 3 causes of hyperchloremia
sodium excess (large and rapid infusions of NS)
bicarbonate deficit
acidosis
what are 4 clinical manifestations of hyperchloremia
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
what is normal osmolarity of plasma
290 mOsm/L
where is hydrostatic pressure the greatest
arterial end of capillary system
aortas
where can hydrostatic pressure build up and cause problems
pulmonary vascular system –> fluid backs up into pulmonary system causing pulmonary edema
where in the vascular system is oncotic pressure the greatest
venous end of capillary system
what solute in our blood is most responsible for maintaining oncotic pressure
albumin
where is the best example of diffusion in the body
gas exchange in the lungs
how does the sodium-potassium pump work
active transport
what does the Na+/K+ pump need to work
ATP!
which hormone causes just water to be reabsorbed back into the bloodstream from the nephrons collecting duct
ADH
which hormones are released as a consequence of the RAA system
aldosterone and ADH
what hormone in the collecting ducts in the nephron to retain sodium and water and excrete potassium
aldosterone
what does adding fluid to a solution do to its concentration
decrease its osmolarity
prior to intervention, a rapidly bleeding patient is experiencing which of the following
isotonic hypovolemia
what would a rapidly bleeding patients hematocrit be
normal
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
increased hematocrit
what state would a patient who was over-rescuitated with plasmalyte and NS be experiencing
isotonic hypervolemia
what state can SIADH cause
hypotonic hypervolemia
an elderly person with communication challenges in long term care is at risk for experiencing what state
hypertonic hypovolemia
which volume and concentration state is induced to treat cerebral vasospasm
isotonic hypervolemia
what medication is given for cerebral vasospasm
nimlodopine Ca2+ channel blocker that works on smooth muscle
what happens when you have blood in the brain regarding CSF
blocks reuptake causing hydrocephalus
receives blood flow from how many sources
2
25% hepatic artery - directly from the blood
75% - portal vein nutrient rich blood from gut, stomach, spleen and pancreas is oxygen poor
what two organs dont go through the liver
legs and kidneys
does blood flow through liver in capillaries
no sinusoids
what are the major functional cells of the liver
hepatocyte
what liver cells conjugate bilirubin
hepatocytes
what do hepatocytes do
perform metabolic, secretory and ednocrine fn
conjugate bilirubin
what cells make up 70% of bodies macrophages
Kupffer cells in liver
What do Kupffer cells do
make up 70% of bodies macrophages
produce cytokines (triggered by endotoxins)
filter bacteria and endotoxins
destroy worn RBC, WBC, and bactera
where are kupffer cells found
in the lining of the sinusoids of the liver
what are 6 fn of the liver
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
What are 3 processes of carbohydrate metabolism in the liver
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
what does the liver do with amino acids
converts them to glucose or lipids
What organ syntehsizes amino acids
liver
what 3 plasma protein are formed in the liver
albumin (60^ of plasma proteins) globulins (immune function) clotting factors (fibrinogen, prothrombin and factors V, VII, IX and X)
what hormone does the liver inactivate
GROWTH HORMONE
What blood vessel does blood flow out of the liver
hepatic vein
what does the liver do with excess carbs and proteins
converts them into fatty acid and triglycerides which are sent out for storage in adipose tissue
What does the liver create cholesterol out of
fatty acids
what does the liver do with trigylcerides
oxidizes them to produce energy
what happens in gluconeogenesis
fats are converted to glycogen and stored for energy
The liver stores what vimtamins
A, D, E and K (fat soluble)
vitamin B12
what minerals are stored in the liver
iron and copper
Where does the body store a back up supply of blood
in the sinusoids of the liver
what hormones does the liver inactivate (6_
aldosterone, cortisol, epinephrine
growth hormone, glucagon, glucocorticoids
what do kupffer cells do
detoxification of drugs and toxins
removes bacteria, antigens and byproducts of coagulation
Where in the body is lactate cleared
liver
what creates ammonia
created in the gut and cells during the breakdown of protein
How is ammonia removed from the body
the liver converts ammonia to water soluble urea
4 ways in which the liver can be acutely injured
Tylenol OD
shock states
viral infection
budd chiari syndrome
what are two chronic causes of liver injury
EtOH and non alcohol liver disease
chronic viral hepatitis (B, C)
why does liver failure cause decreased LOC
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
why does liver failure cause bleeding
unable to creat clotting factors
portal HTN causes the formation of variceis
unable to store vitamin K
why does liver failure cause edema,a sites, leaking wound sites
unable to create albumin causing decreased oncotic pressure (unable to pull fluid)
backflow of blood from damaged liver
why does liver failure cause jaundice
unable to conjugate bilirubin and excrete it so you have excess bilirubin
why does liver failure lead to increased chance of infection
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
why does portal HTN occur in liver failure
liver becomes cirrhosed and blood is unable to flow through it
why does hypoglycemia occur in liver failure
unable to perform glycogenolysis and gluconeogenesis
impaired carbohydrate metabolism
What are LFTs
AST, ALT, Albumin, PT/INR, alk phos, GGT, bilirubin, ammonia, platelets
What is AST? where is it found? is it specific for the liver?
asparate aminotransferase
found in the liver, heart, skeletal muscle, pancrease and kidneys
low specificity to the liver
What enzyme found in hepatocytes is most specific to the liver
ALT
Does decreasing ALT/AST mean that your pts liver is improving
not necessarily, could mean that your pateints liver injury has progressed to the point they have few functioning hepatocytes
What does albumin tell us
chronic liver failure indicator as albumin has a long half life of 20 days
what is a good indicator of chronic liver injury
albumin
is albumin specific
no a decrease could be liver, could be leaking out such as sepsis or trauma or could be malnourished
What is a very sensitive indicator of liver dysfunction that is often the first to be affected
PTT and INR since the liver synthesizes so many clotting factors
is alk phos able to tell us liver function on its own?
no need GGT as well
what is alk phos? where is it commonly found?
what is is most specific for on its own
alkaline phosphatase
found in may tissues mostly bone and liver
most specific for bone disease
what is GGT? what does it do? where is it found? Where is it most concentrated?
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
if you have a high alk phos and GGT what does this mean
liver porblem
if you have a high alk phos and normal ggt what does this mean
bone problem
Why do we check platelet levels in our LFTs
liver produces thrombopoietin which tells the bone marrow to increase platelet production
What is refeeding syndrome
potential fatal shift in fluid and electrolytes that occurs when re-introducing malnourished patients to any form of nutrition
what time frame does re-feeding syndrome occur in
12-72 hours after refeeding is initaited
how long can refeeding syndrome continue for
2-7 days
what are three things that occur during times of malnourishment
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
what occurs when we start refeeding malnourished patients
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
what specifically causes edema to occur in refeeding syndrome
sodium moving out of the cell as K+ moves in
what is the main electrolyte imbalance that is a hallmark sign of refeeding syndrome
hypophosphatasemia
What are 5 signs of refeeding syndrome
hypophosphatemia abnormalities in fluid balance vitamin deficiency e.g. vitamin B1 (thiamine) hypomagnesaemia hypokalemia
what can the electrolyte and fluid balance abnormalities in refeeding syndrome cause
cardiac, respiratory and neuromuscular consequences
how do we start feeding pts suspected of refeeding syndrome
slowly
what should we monitor for refeeding syndrome
blood work closely and replacement of electrolytes
What is thiamine absolutely necessary for
ATP
what are three things that occur with low thiamine
muscle weakness
Wernicke syndrome
HF
