1/64
Looks like no tags are added yet.
Name | Mastery | Learn | Test | Matching | Spaced | Call with Kai |
|---|
No analytics yet
Send a link to your students to track their progress
Intracellular fluid (ICF)
about 2/3 of total body water
located within the cells
potassium is the chief cation
phosphate is the chief anion
Extracellular fluid
about 1/3 of total body water
located outside of cells
sodium is the chief cation
chloride is the major anion
The ECF is divided into plasma and interstitial fluid
Plasma (ECF)
fluid portion of the blood
Interstitial fluid (ECF)
fluid in the spaces between cells
other extracellular fluids are present in small amount and are considered IF
lymph, cerebrospinal fluid, eye humors, Synovial fluid, etc
Water
is the universal solvent
solutes are broadly classified into two types
Electrolytes
charged particles
include salts, acids, bases
measured in mEq/L when assessing charge
have greater osmotic power because they form particles in solution
Non-electrolytes
do not dissociate into ions (no charge)
ex. glucose, lipids, creatinine, urea
measured in concentration units or osmolality
Osmosis
water moves according to osmotic gradients
movement is toward areas with higher solute concentration
determined by the number of particles in solution, not change
Milliequivalents (mEq)
reflect the amount of charge
charge maintains electrical neutrality in body fluids
Milliosmoles/liter (mOsm/L)
reflect the concentration of particles
this determines osmosis
Monovalent ions (Na+,K+)
1mEq=1mOsm
Divalent ions (Ca2+)
1mEq=0.5mOsm
Ca2+ carries more charge per particle, so fewer particles are needed to get the same electrical effect
Capillary exchange (plasma ←→ IF)
driven by Starling forces, maintains plasma volume and prevents edema
at the arterial end the hydrostatic pressure is greater than the oncotic pressure allowing for filtration
at the venous end the oncotic pressure is greater than the hydrostatic allowing for reabsorption
Cell exchange (IF←→ICF)
water shifts rapidly via osmosis, driven by solute concentration
ions are regulated by channels and pumps (ex. Na+K+ATPase)
nutrients diffuse or are transported into cells
metabolic wastes diffuse out to IF then blood then excretion
gas exchange driven by partial pressure gradients
Hypertonic (Increased ECF osmolarity)
water leaves the cell causing it to shrivel
Hypotonic (decrease ECF osmolarity)
water enters the cell and swells
Water intake sources
fluids 60%
food 30%
metabolic production 10%
Water output
urine 60%
feces 4%
lungs 28%
skin 8%
Dehydration
increased ECF osmolarity causes water shifts out of the cell
Na+ is the primary determinant of ECF osmolarity
Hypotonic/Over hydration
decreased ECF osmolarity causes dilutuinal hyponatremia
water is driven into the cells
cellular swelling poses a greater risk in the brain for cerebral edema and for RBC damage
commonly caused by the impairment of ADH
Edema (interstitial fluid accumulation)
results from imbalance of capillary forces or lymphatic drainage
results in decreased plasma volume and blood pressure
Edema mechanisms
increased capillary hydrostatic pressure increases filtration
decreased plasma oncotic pressure decreases reabsorption
lymphatic obstruction decreases the amount of fluid returned to circulation
Causes of edema
hypoproteinemia (malnutrition and liver disease can cause low oncotic pressure)
venous congestion from heart failure
lymphatic blockage or removal
Thirst regulation
hypothalamic thirst center drives water intake
Stimuli for thirst
increased ECF osmolarity is the primary trigger
decreased blood volume or pressure is another trigger
Inhibition of thirst
mositening of mouth and throat
stretches of stomach and intestines
Water regulation by ADH
increased ADH allows for increased water reabsorption, causing concentrated urine and a high ECF volume (your body is keeping the water not peeing it out)
decreased ADH causes decreased water reabsorption causing diluted urine and a low ECF volume (your body is peeing out the water)
Water regulation by aldosterone
increased Na+ reabsorption, water follows, increasing ECF
effect depends on presence of ADH
Hypernatremia
excess Na+ or water loss
Hyponatremia
Na+ loss or excess water
Sodium regulation by aldosterone
increased Na+ reabsorption in the kidneys causes increased ECF volume
ANP/BNP are released with cardiac stretch and increase Na+ excretion in order to lower ECF volume
Hyperkalemia
too much potassium
Hypokalemia
too little potassium
Potassium regulation and aldosterone
stimulated by increased K+
increases K+ secretion in the kidneys to lower the levels
Potassium and Acidosis
H+ enters the cell as K+ exits
causing an increase in plasma K+ ions
Potassium and alkalosis
H+ exits the cells as K+ enters
causing a decrease in plasma K+
Insulin and potassium
insulin stimulates Na+K+ATPase, causing K+ to shift into cells
decreases serum K+
insulin can be used to treat hyperkalemia rapidly
given with glucose often to prevent hypoglycemia
Hypocalcemia
too little Ca2+
Hypercalcemia
too much Ca2+
Calcium regulation
Parathyroid hormone raised Ca2+ and is released in response to low Ca2+
increases Ca2+ via bone resorption, renal reabsorption and intestinal absorption
Calcitonin lowers Ca2+ by inhibiting bone resorption
Acidosis
pH < 7.35
Alkalosis
pH > 7.45
Carbon dioxide as a regulator
normal: 40-45 mmHg
forms carbonic acid which decreases pH
Bicarbonate as a buffer
normal: 22-26 mEq/L
buffers H+ to increase pH
Chemical buffers (seconds)
regulated H+ concentration with an immediate response
bind or release H+ (ex. HCO3- buffer system)
Respiratory system (minutes)
H+ concentration is controlled by brainstem (ventilation control)
Renal system (hours)
regulates H+ and HCO3-
Chemical buffers systems
resist changes in pH
bind H+ when pH is low
release H+ when pH is high
Bicarbonate buffer (ECF)
most important
lungs regulate CO2, kidneys regulate HCO3-
Phosphate buffer (ICF)
more important inside cells
Protein buffers
proteins bind or release H+
ex. hemoglobin
Respiratory acid base balance
CO2 driven
Metabolic acid base balance
HCO3-
Respiratory acidosis
hypoventilation leads to CO2 retention
cause: opioid overdose, falling asleep and the brain shuts down the automatic center causing CO2 to build up
cause: COPD, asthma, pneumonia, directly impact the lungs (hypoventilation)
compensation: urine becomes more acidic
Respiratory alkalosis
hyperventilation leads to excessive CO2 loss
causes: anxiety, sobbing, pain
compensation: urine becomes less acidic
Metabolic acidosis
increased H+ or decreased HCO3-
causes: diabetic ketoacidosis, fatty acids causes keystones and the liver produce acidix keytones for energy
causes: diarrhea, loss of HCO3-
compensation: increase ventilation
Metabolic alkalosis
increased HCO3- or decreased H+
causes: vomiting, throw up stomach acid, stomach needs more acid so it pulls H+ out of the blood
compensation: decrease ventilation
Lungs fix metabolic
Kidneys fix respiratory