Exam 1: Ch 8 Flashcards
extracellular fluid
interstitial fluid and plasma
mEq
milliequivalents
mEq/L = # of millimoles of charges/L = (mg/L x valence) / AW
mMol/L = # of millimoles of particles/L = (mg/L) / AW = (mEq/l) / valence
is osmosis water moves to the side…
with more solute particles
measures as mOsm/L or osmolatity
extent of osmotic pressure measured by…
mOsmoles = mMol of non-diffusable particles
tonicity
effect of osmotic pressure on a cell
hypotonic solutions have > osmolarity than the cell (swell)
hypertonic solutions have < osmolarity than the cell (shrink)
distribution of body fluids
total body water: 60% of weight
intracellular fluid is 2/3, extracellular 1/3
interstitial fluid is 2/3 of extracellular (rest is plasma, and transcellular fluid)
transcellular fluid
CSF
peritoneal
pleural
capillary filtration pressure (hydrostatic pressure)
BP in a capillary
higher at arterial end than venous end
outward force - pushes blood into interstitium
interstitial fluid pressure
low but normally negative
outward force
interstitial colloid osmotic pressure
low
outward force
capillary colloid osmotic pressure
mostly from proteins (albumin made in liver) in plasma
electrolytes pass freely, no net pressure
inward force - pulls blood back into veins
exchange in capillaries
at arterial end out > in, net filtration
at venous end in > out, net reabsorption
fluid or protein not reabsorbed, returns to circulation in lymph
edema
swelling caused by excess interstitial fluid
increased capillary filtration (hydrostatic) pressure
more fluid leaves capillary space
usually from increased venous pressure (HF) or increased pressure at arterial end of capillary
decreased capillary colloid osmostic pressure
causes edema
less fluid returns to capillary (low albumin)
liver failure or heart disease
increased capillary permeability
causes edema
plasma proteins leak out of capillaries
inflammation
obstructed lymph flow
causes edema
prevents return of proteins and fluids to circulation
malignancy or surgery
assessment/treatment of edema
weight, visual assessment, measurement of affected part
elevate lower extremities, support stockings, diuretics
third space fluid accumulation
trapping in transcelular space
peritoneal, pleural, or pericardial
may require drainage
TBW of water in lean adults vs. infants
60% lean adults
75-80% in infants
how is water taken in and excreted?
intake: drink, food, metabolism
output: urine, respiratory, skin, feces
regulation of Na balance
most plentiful extracellular cation
intake: GI
output: renal, skin, lungs
RAAA system
renin angiotensin-aldosterone system
lowers sodium concentration, blood volume
BP activates
ADH stimulates ____ ____ while Aldosterone stimulates ____ ____
water retention
sodium retention
released together
aldo effect and ADH effects
aldo: increased urinary Na retention
ADH: increase thirst –> increase H2O intake & decreased urine water loss
if low BP (and low blood volume) due to ECF fluid loss and/or Na loss
renin and angiotensin II released and activated
increase aldo and ADH release
if high BP and high blood volume due to excess ECF and or Na gain
increased NP release
decrease aldo and ADH release
thirst controlled by
thirst center in hypothalamus, which has osmoreceptors
ADH released by hypothalamus to retain water if ECF is low or there is cellular dehydration
hypodipsia
decreased ability to sense thirst
lesions on hypothalamus
polydipsia
excessive thirst
CRF or HF from high angiotensin
true thirst
accompanies dehydration from blood loss or diabetes mellitus
psychogenic polydipsia
compulsive drinking in psychiatric disorders
2 ADH disorders
diabetes insipidus
syndrome of inappropriate ADH secretion
2 types of diabetes insipidus and definition in general
decreased ADH, leading to high urine output, dehydration, and high serum sodium (only losing H2O, not ions)
neurogenic
nephrogenic
neurogenic diabetes insipidus
caused by trauma, solve with ADH administration
decreased ADH, leading to high urine output, dehydration, and high serum sodium (only losing H2O, not ions)
nephrogenic diabetes insipidus
renal response off ADH decreased
decreased ADH, leading to high urine output, dehydration, and high serum sodium (only losing H2O, not ions)
what does ADH do cellularly
inserts aquaporins that are impermeable to ions
causes H2O to leave urine and enter the blood, causing low serum Na (diluted by the H2O)
decreases urine output
syndrome of inappropriate ADH secretion
causes dilutional hyponatremia
tumor can secrete extra ADH
treat with diuretics and fluid restriction
physiological effects of dilutional hyponatremia caused by syndrome of inappropriate ADH secretion
reabsorb H2O so low urine output
low serum sodium
high BP
isotonic fluid volume deficit
loss of isotonic fluid from ECF
ICF not impacted
causes, symptoms, and treatment of isotonic fluid volume deficit
causes: vomiting, diarrhea, NG suction
symptoms: thirst, weight loss, oliguria, increased urine specific gravity
treatment: correct problem and administer isotonic fluid
isotonic fluid volume excess
gain of isotonic fluid into ECF
ICF not impacted
causes, symptoms, and treatment of isotonic fluid volume excess
causes: renal or HF, corisol excess
symptoms: weight gain, edema, distended neck veins, pulmonary edema, ascites
treatment: sodium restriction and diuretics
hyponatremia
low serum Na of less than 135 mEq/L and low serum osmolarity
results from loss of Na in excess of (or without) H2O loss and gain of H2O without sodium
causes, symptoms, and treatment of hyponatremia
SIADH, renal disease that increases water retention
neuro (headache, disorientation), muscle cramps, weakness
limit H2O intake, give hypertonic sodium solutions if sever
water enters ICF by _____
osmosis
produces cellular edema (includes cerebral edema)
hypernatremia
serum Na less than 145 mEq/L and serum osmolarity > 295 mOsm/L
results from gain of sodium or loss of H2O
causes, symptoms, and treatment of hypernatremia
lack of H2O access, hypodypsia, excess sodium bicarb
weight loss, polycythemia, thirst, neuro symptoms
give rehydration fluids –> slowly to avoid cerebral edema
water leaves ICF by ____
osmosis
causes cellular dehydration
normal serum volume of potassium
3.5-4.5 mEq/L
regulation of potassium balance
renal regulation: K+ filtered and partially reabsorbed
excretion fine tuned by aldosterone-sensitive sodium reabsorption/potassium secretion in DCT
how are Na/K gradients maintained
Na/K ATPase pump
cellular dehydration –> increase K shift out of cells
intracellular acidosis –> increase K shift out of cells
Insulin and Epi stimulate pump –> increase K movement into cells
2 disorders of potassium imbalance
hyperkalemia
hypokalemiaq
hyperkalemia effect on resting membrane potential
reduces ratio so RMP is closer to threshold for AP
hypokalemia effect on resting membrane potential
increases ratio so RMP is further from threshold for AP
hyperkalemia
K+ > 5 mEq/L
causes: decreased renal elimination (CRF), increased movement from ECF (acidosis)
symptoms: peaked T wave, short QT, wide QRS!!!! weakness and muscle cramps
treat: CaCl2 to reverse ECG changes, beta-agonists, insulin
hypokalemia
K+ < 3.5 mEq/L
causes: decreased intake, vomiting, diarrhea, renal loss (diuretics), shifts into cells (epi & insulin), treatment of ketoacidosis
symptoms: PR prolonged, premature ventricular contractions, weakness, fatigue, muscle cramps
treat: replace with IV rapidly if needed
2 regulators of calcium
PTH increases calcium
calcitonin decreases calcium
PTH
increases calcium
increased absorption by gut (Vit D)
decreases renal elimination
stimulates osteoclasts (breakdown of bone)
calcitonin
decreases calcium
2 PTH disorders
hyperparathyroidism
hypoparathyroidism
hyperparathyroidism
excess PTH –> high calcium
parathyroid adenoma
skeletal abnormalities that may be asymtomatic
hypoparathyroidism
PTH deficit so low calcium
congenital absence of gland, acquired (surgery or radiation)
symptoms: tetany, prolonged QT
treat: IV calcium gluconate, Vit D
most calcium stored in ____
bone
calcium in ECF
1/2 calcium bound to albumin and 1/2 free
hypocalcemia
serum calcium less than 8.5 mg/dL
treat: replace calcium
causes and symptoms of hypocalcemia
causes: renal loss (failure) and hypoparathyroidism
symptoms: nerve and muscle excitability, tingling, spasms, and seizures b/c Ca stabilizes membranes
2 signs of hypocalcemia
Chvostek: contracture of facial muscles from light tap
Trousseau: carpal spasms from inflating BP cuff
hypercalcemia
serum calcium greater than 10.5 mg/dL
causes: bone resorption (cancer) and hyperparathyroidism
symptoms: decreased neural exitability
regulation of magnesium balance
reabsorption in DCT stimulated by PTH
hypomagnesemia
serum Mg less than 1.8 mg/dL
caused by diarrhea, malabsorption, laxatives
symptoms: tachycardia and HTN
hypermagnesemia
serum Mg greater than 2.6 mg/dL
caused by renal disease, and magnesium containing meds like antacids
symptoms: hypotension and cardiac arrest
why is pH important
enzymes are sensitive
cardiac and neural function is decreased when pH is low
acids are generated by ________
metabolism
fixed acids
sulfuric
phosphoric
lactic
ketone bodies
sulfuric and phosphoric acid
produced in metabolism of AA, NA, and phospholipids
excreted by kidney
lactic acid
from pyruvic acid in anaerobic metabolism
ketone bodies
from fat and protein during catabolism
volatile acid
CO2
end product of aerobic metabolism
H2O + CO2 –> H2CO3 –> H+ + HCO3-
high pCO2
acidosis
low pCO2
alkalosis
3 lines of defense against acidosis/alkalosis
1: chemical buffering
2: respiratory response by breathing out CO2
3: renal response
CO2 is produced in ____ and diffuses into ____
cells, plasma
CO2 in RBC and enzyme
H2O + CO2 –> H2CO3 –> H+ + HCO3-
by carbonic anhydrase
CO2 is carried in 3 forms
bicarb 70%
dissolved in plasma 10%
bound to hemoglobin 20%
calculation of pH
Henderson-Hasselbach
rate of bicarb to CO2 determines pH
pH = 6.1 + log [HCO3-] / (.03 * pCO2)
the log of a bigger # = a
bigger #
causes of acidosis bicarb/CO2
low biarb
high CO2
causes of alkalosis bicarb/CO2
high bicarb
low CO2
buffer systems
1st line of def
bicarbonate buffer system most important
H2O + CO2 –> H2CO3 –> H+ + HCO3-
if high pH, moves to right to release H+
if low pH, moves to left to absorb H+
protein buffer systems
albumin and globulins (major plasma proteins)
potassium H+ ion exchange
in metabolic acidosis H+ inc. in cells so K+ moved out
treatment of ketoacidosis requires K+ replacement
respiratory control of CO2
2nd line of def
increased production of metabolic acids or CO2 stimulates chemoreceptors
respiratory centers are stimulated to increase minute respiration (breathe more CO2 out to inc. pH)
rapid response… 12-24 hrs
acidosis means you breathe…
harder
alkalosis means you breathe
slower
renal control mechanisms
3rd line of def
kidney changes excretion of acid or base to compensate for pH changes
H+/bicarb exchange (requires carbonic anhydrase)
H+/bicarb exchange
H+ ions secreted into tubular fluid in exchange for Na
bicarb reabsorbed into blood
stimulated by acidosis
diamox
diuretic and carbonic anhydrase inhibitor
moves Na into urine and H2O follows
tubular buffer systems
prevent urine from becoming too acidic (excretes H+ ions)
phosphate buffer system
ammonia buffer system…. NH4+ produced and secreted and NH3 acts as buffer
lab tests for acid/base abnormalities
use arterial blood
pH and pCO2 measured, bicarb calculated
interpretation of lab acid/base tests
pH determines acidosis or alkalosis
if abnormal CO2, problem is respiratory
if abnormal HCO3-, problem is metabolic
_____ system can adjust CO2 to compensate for a _____ disorder
respiratory, metabolic
_____ system can adjust HCO3- to compensate for a _____ disorder
renal, respiratory
is mixed acidosis/alkalosis possible?
yes
anion gap
serum concentration of unmeasured anions (phosphate, sulfate, organic acids, protein)
calculated as sodium - (chloride + bicarb)
use to confirm diagnosis
anion gap is increased in…
lactic acidosis
ketoacidosis
b/c large amounts of lactate and ketone present (anions)
anion gap is normal from ______
diarrhea
Cl retained as bicarb is lost
anion gap is decreased in…
hypoalbuminemia
