Ch 24 patho F&E
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Where does the ECF lie?
- interstitial - between the cells
- vascular - in blood vessels
- transcellular - in dense connective tissue and bone
4 materials that ICF is rich in?
- 1. K+
- 2. Mg
- 3. phosphates
- 4. proteins
2 materials ICF is low in?
na and cl
ECF is relatively high in ___, ___, & ____ ions and relatively low in ____, ____, & ____ ions.
Na, Cl, and bicarbonate
K+, Mg, and phosphate ions
What happens to an infants body weight as they get older?
it goes down
Why do women have less percentage of water in their body than men?
muscle holds more water than fat
4 processes that control fluid homeostasis?
- 1. fluid intake
- 2. fluid excretion
- 3. fluid distribution
- 4. fluid absorption
3 factors that influence oral fluid intake?
habit, social, and thirst
3 Physiologic triggers of thirst?
- 1. increased osmolality of ECF
- 2. decreased circulating blood volume
- 3. dry mucous membranes of the mouth
What causes older adults to not take in enough fluids?
cerebral osmoreceptor-mediated thirst diminishes with age
What controls fluid distribution b/t caps and interstitial spaces?
hydrostatic pressure and osmotic pull of electrolytes on either side pull water by filtration
fluid moves back and forth depending on net force exerted in caps or in interstitial spaces
What controls the distribution of fluid b/t interstitial and intracellular compartments?
osmosis - simple diffusion of water in response to osmolality differences inside and outside the cell
4 ways fluid is excreted?
urinary, GI, lungs, and skin
3 hormones that control fluid excretion in the urinary system?
ADH, aldosterone, and natriuretic peptides
ADH is released from the ___ ____ ____.
What stimulates its release/inhibits its release?
What does it do when released?
anterior pituitary gland
stimulated by increased osmolality of the ECF, decreased circulating fluid volume, pain, N, and physiologic and psychological stressors
inhibited by decreased osmolality of the ECF & ethanol intake
circulates to distal tubules and cllecting ducts in kidneys where it causes reabsorption of water that dilutes the blood and other body fluids causing urine to be concentrated
Aldosterone is synthesized and secreted by cells in the ____ ____.
Stimuli for its release?
angiotensin II & increased concentration of K+ ions in the plasma
causes renal tubules to reabsorb sodium and water & expand ECF volume, decreases urine volume
Difference b/t aldosterone and ADH?
ADH causes reabsorption of water and aldosterone causes reabsorption of water and Na
Where are ANP and BNP stored?
What stimulates their release?
ANP - cardiac atrial cells - released in response to atrial stretching
BNP- ventricular cells - released in response to ventricular diastolic pressure increases (heart failure)
Effects of the release of ANP & BNP?
promote fluid excretion in the urine by causing excretion of Na accompanied by water
Na excretion in the urine
What effect do natriuretic peptides (ANP & BNP) have on blood volume?
when blood volume is high and heart is stretched ANP & BNP are released and more Na and water are excreted, decreasing blood volume
when blood volume is low they are not excreted and more water is absorbed
not enough fluid volume in ECF, but the concentration is normal
Causes of ECV?
any losses from GI that are not normal, renal impairments where salt is lost along with water, hemorrhage, diaphoresis, third space fluid accumulation (any fluid retained in an area of the body its not supposed to be in), procedures where ECF is removed, burns
Manifestations of ECV defecit?
same as dehydration
one liter of saline weighs ____kg.
If a person loses a kg in 24 hours they have lost ___ L of ____.
1 liter of fluid
When may fluid loss not cause weight loss?
if fluid is going into third spaces
vascular and interstitial areas have toomuch isotonic fluid
Causes of ECV excess?
anything that causes body to retain Na & water - aldosterone excess, heart probs, kidney probs, etc
S/S of ECV excess?
sudden weight gain, edema, and manifestations of circulatory overload, bounding pulse, neck vein distention, crackles, dyspnea, orthopnea, frothy sputum of pulmonary edema, bulging fontanel
How ar imbalances in of body fluid concentration assessed?
body fluids have too much water and not enough Na
Causes of hyponatremia?
anything that increases water or decreases Na: excess ADH release (retains water but not Na), more water than kidney can excrete, heavy sweating (lose more salt than water),
Clinical manifestations of hyponatremia?
nonspecific manifestations of CNS dysfunction: malaise, anorexia, nausea, vomiting, HA, confusion, lethargy, seizures, and coma
What can profound hyponatremia cause
fatal cerebral herniation
What causes the symptoms of hyponatremia?
swelling of neurons and glial cells as a result of decreased osmolality of extracellular fluid
Who is most at risk for hypernatremia? Why?
older adults b/c they gain relatively more solute than water
S/S of hypernatremia?
same as hyponatremia with thirst or oliguria
combo of ECV deficit and hypernatremia
excess of fluid in the interstitial compartments
increase in forces that move water out of caps or decrease in forces that move water out of interstitial spaces into caps
3 factors that increase cap hydrostatic pressure?
- 1. increased ECV
- 2. increased local cap flow that accompanies inflammation
- 3. venous congestion
What can increase interstitial fluid osmotic pressure?
INFLAMMATION INCREASES VASCULAR PERMEABILITY AND PROTEINS LEAK INTO THE INTERSTITIAL FLUID or blockage of lymphatic drainage that normally removes these proteins
What causes decreased cap osmotic pressure/
concentration of plasma proteins is decreased: malnutrition or liver disease (protein synthesis)
7 most important electrolytes?
Na, Ca, K, Cl, Mg, bicarbonate, phosphate
What electrolyte has an IM injection?
What are 4 things that can decrease absorption of electrolytes taken in orally?
- 1. concentration gradients can decrease K
- 2. Ca and others depends on availability of binding proteins
- 3. contents of the GI tract such as fat can bind them so they can't be absorbed
- 4. surgical removal of portions of the GI tract
The concentrations of ___, ___,& ____ ions are higher inside cells than in the fluid outside the cells.
K, Mg, and phosphate
Explain the concentration of Ca in ICF & ECF.
There is more Ca in the ICF, but it is bound to other molecules so there is a higher concentration of active Ca in the ECF
The bones are a reservoir for what 3 electrolytes?
CA, Mg, and phosphate
How is the shifting of electrolytes b/t ECF & ICF controlled?
Epinephrine effects what electrolyte's concentrations?
What hormone effects K and phosphate ion concentrations?
What hormone effects Ca concentrations?
What hormone increases K excretion?
Medications that increase K excretion?
Drugs that increase Mg excretion?
diuretics & aminoglycoside antibiotics (gentamicin)
Drug that increases Ca excretion?
thiazide diuretics (HCTZ)
Diarrhea increases the excretion of ___ &____ ions in particular
K & Mg
How does undigested fat in the intestines affect ions lost in feces?
binds to Ca and Mg so they cannot be absorbed and are excreted in feces
decrease in concentration of K ions in the blood serum but not necessarily in ICF or other areas of the body
Causes of hypokalemia?
factors that decrease K intake, shift K from ECF into the cells, increase K excretion, cause K loss from body by abnormal route: diretics, corticosteroids, aldosterone, heart failure, cirrhosis
What type of candy can cause hypokalemia?
Clinical manifestations of hypokalemia?
altered function of all muscles due to hyperpolarization and decreased reaction to stimuli in cells - abd distention, diminished bowel sounds, paralytic ileus, postural hypotension, skeletal musc weakness, flaccid paralysis, cardiac dysrhythmias
3 conditions that can occur due to chronic hypokalemia?
- 1. rhabdomyolysis - skeletal muscle b/d
- 2. selective myocardial cell necrosis
- 3. nephropathy
skeletal muscle b/d
Causes of hyperkalemia?
blood transfusion, K shifting form cells to ECF, decreased K excretion from kidneys without an adjustment in dietary intake of K (oliguria)
Clinical manifestations of hyperkalemia?
hypopolarized smooth and skeletal muscle cells - intestinal cramping and diarrhea,
skeletal muscle cells may become so hypopolarized that their resting membrane potentials lie above their threshold potential and they are unable to contract
cardiac mus are hypopolarized: rate of rise of cardiac action potentials decreases conduction velocity in the heart = cardiac dysrhythmias & cardiac arrest
2 mechanisms of hypokalemia adaption?
- 1. aldosterone levels increase= increased K excretion by the colon
- 2. shift K ions from ECF to ICF to normalize resting membrane potentials
3 forms of Ca in the plasma?
- 1. Ca bound to plasma proteins (albumin)
- 2. Ca bound to small organic ions (citrate)
- 3. unbound Ca
What condition increases fat in the intestine and decreases Ca absorption?
pancreatitis - lack of pancreatic lipase in the intestines causes undigested fat to build in intestines and bind to Ca decreasing its absorption
Function of parathyroid hormone in Ca concentration?
increases plasma Ca concentration
Clinical manifestations of hypocalcemia?
increased neuromuscular excitability, positive Trousseau sign, postivie Chvostek sign, paresthesias, muscle twitching and cramping, hyperactive reflexes, carpal spasm, pedal spasm, tetany, larygospasm, seizures, and cardiac dysrhythmias
Effects of hypocalcemia on the heart?
impaired atrioventricular and intraventricular conduction and impaired myocardial contractility = heart failure
Positive Trousseau sign?
occurrence of a carpal spasm after occlusion of arterial blood flow to the hand for approx. 3 minutes
Positve Chvostek sign?
spasm of muscles in the cheek and corner of the mouth produced by tapping facial nerve in front of the ear
______ causes more Ca to be shifted out of bone and can cause hypercalcemia if it is released excessively.
Clinical manifestations of hypercalcemia?
decreased muscular excitability, anorexia, nausea, emesis, constipation, fatigue, polyuria, muscle weakness, diminished reflexes, HA, confusion, lethargy, peronality change, and cardiac dysrhythmias
Effects of hypercalcemia on muscle cells?
decreased neuromuscular excitability caused by elevation of the threshold potential of excitable cells
hypercalcemia cardiac effects?
shortened plateu phase of action potential, increased rate of diastolic depolariaztion of sinus node cells and delayed atrioventricular conduction
Effects of hypercalcemia on renal function and bones?
causes bone resorption and may lead to pathologic fractures
Causes of hypomagnesemia?
What other electrolyte may become depleted along with hypomagnewsemia?
K due to increasing urinary excretion
Clinical manifestations of hypomagnesemia?
excessive release of acetylcholine that is normally depressed by Mg ions causes increased neuromuscular excitability: insomnia, active reflexes, muscle cramps, muscle twitching, grimacing, positive Chvostek sign, positive Trousseau sign, nystagmus, dysphagia ,ataxia (noncoordinated muscular movements), tetany, and seizures
Causes of hypermagnesemia?
hyperparathyroidism shifting Mg from bones to ECF, excessive intake of Mg in laxatives and antacids, oliguria,
What 2 groups of ppl are at high risk for hypermagnesemia?
- 1. older adults who take Mg containing meds
- 2. ind who have oliguria (chronic renal failure)
Clinical manifestations of hypermagnesemia?
dpressed neuromuscular function by decreasing release of acetylcholine at neuromuscular junction: decreased depp tendon reflexes, lethargy, hypotension, flushing, diaphoresis, drowsiness, flaccid paralysis, resp depression, bradycardia, cardiac dysrhythmias, and cardiac arrest
What mechanisms cause cardiac effects of hypermagnesemia?
decreased cardiac conduction and depression of membrane excitability
Clinical manifestations of hypophosphatemia are usually not observed unless the levels drop below _____ mg/dl.
Causes of hypophosphatemia?
any factor tha causes rapid increase in cellular metabolism causes phosphate to shift form ECF into cells, chronic alcoholism, chronic diarrhea,
What pt's are especially at risk for hypophosphatemia?
pt who are severly malnourished after nutritional replacement is started b/c of their increased cellular metbolism and previously depleted phosphate stores
What causes the Clinical manifestations of hypophosphatemia?
mostly decreased amounts of ATP b/c phosphate is an important component of ATP
also hypoxia b/c of decreased amnts of 2,3-biphosphoglycerate in the red blood cells
S/S of hypophosphatemia?
anorexia, malaise, parestheisas, hemoluyis, diminished reflexes, muscle aches, muscle weakness, resp failure, confusion, stupor, seizures, coma, and impaired cardiac function
Effects of hypophosphatemia on cardiac function?
decreased cardiac contractility and stroke work concurrent with increased left ventricular end-diastolic pressure and may cause congestive heart failure
Causes of hyperphosphatemia?
oliguric renal diseaseelevate parathyroid hormone shifts phosphate from bones into ECF
What causes Clinical manifestations of hyperphosphatemia?
effect of the elevated phosphate ion concentration on Ca ions
S/S of hyperphosphatemia?
hypocalcemia, s/S same as hypocalcemia as well as deposition of Ca phosphate salts in soft tissues of the body: aching and stiffness in joints, pruritus, and conjuctivitis depending on where Ca phosphate is deposited
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