alterations in fluid and electrolytes Chapter 8

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Last updated 11:27 PM on 9/10/23
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75 Terms

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intracellular fluid compartment
makes up 2/3
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extracellular fluid compartment
makes up 1/3
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intracellular water of body weight
makes up 40%
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extracellular water of body weight
makes up 20%
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electrolyte
substances that dissociate in solution to form charged particles
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what does ECF have lots of?
lots of sodium and chloride
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what doesn’t ECF have lots of
little Potassium
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what does ICF have lots of?
lots of potassium
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what doesn't ICF have lots of?
little sodium and chloride
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Osmosis
movement of water down its concentration gradient \n across a semipermeable membran
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increase in ECF osmolarity
water leaves the cell
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decrease in ECF osmolarity
water enters the cell
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tonicity
tension or effect a solution with impermeable solutes exerts on cell size due to water movement across the cell membrane
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what does water always move from?
low to high osmotic pressure
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capillary filtration pressure (hydrostatic)
pushes water out of capillary and into tissue
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capillary colloidal /osmotic pressure
pulls water into capillary from tissue
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interstitial hydrostatic pressure
pushes water out of tissue and into capillary
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interstitial colloidal osmotic pressure
pulls water into tissue and out of capillary
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hydrostatic pressure
pushes fluid into something
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colloidal osmotic pressure
pulls fluid into something
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interstitial pressures
pushes fluid in and out of something
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lymph system
accessory system where fluid is returned to the circulatory system
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edema
palpable swelling produced by an increase in interstitial fluid volume
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increased capillary filtration pressure
Increased vascular volume \n • Heart failure, kidney disease \n • Hormone-related sodium retention, pregnancy \n • Venous obstruction \n • Liver disease, pulmonary edema, venous \n thrombosis
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decreased capillary colloidal pressure
Increased loss of plasma proteins (burns, \n glomerular basement membrane injury) \n • Decreased plasma protein production (liver \n disease, malnutrition, starvation
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increased capillary permeability
Inflammation, allergic reactions \n • Tissue injury and burns
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obstruction of lymph flow
Malignant obstruction \n • Removal of lymph nodes
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manifestations of edema
life threatening : brain, lungs, and larynx

impairs movement and discomfort

tissue level : impairs diffusion of oxygen, nutrients, and waste which increases damage
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pitting
fluid exceeds absorptive capacity
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edema- assessment
daily weights, visual inspection, and pitting ed
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edema treatment
elevation, diuretics, and albumin replacements if needed
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third spacing
considerable enlargement of transcellular fluid compartment (fluid is trapped)
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ascites
accumulation of fluid in peritoneal cavity
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total body water
varies by body composition

increase in lean muscle mass and infants

decrease with age and obesity
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sodium
normal levels: 135-145

primary loss through kidneys

big loss through vomitting and diarrhea

little loss through GI and skin
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effective circulating volume
monitored by sensors in vascular system and kidneys
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baroreceptors
respond to pressure-inducted stretch of vessel walls
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mechanisms of water and sodium regulation
ADH

SNS

RAAS

ANP
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high osmolarity leads to
increase thirst

release of ADH
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low osmolarity leaves to
lack of thirst

decreased ADH release
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hypodipsia
decrease in ability to sense thirst
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polydipsia
excessive thirst
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true thirst
loss of body water and resolves with fluid replacement
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false thirst
occurs with chronic diseases, dry mouth, medications
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psychogenic
compulsive-schizophrenia
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what does ADH controls ?
resorption of water by the kidneys
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diabetes insipidus
insufficiency of ADH

partial or total inability to concentrate the urine that increases plasma osmolarity resulting in hypertonic dehydration

\-enhanced water excretion

\-hypernatremia

\-serum hyperosmolarity

decrease in H2O and increase in osmolarity
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syndrome of inappropriate antidiuretic hormone secretion
hypersecretion of ADH

\-enhanced renal water retention

\-hyponatremia

\-sereum hypo-osmolarity

low urine output, GI symptoms, dulled senses, mental changes

increase in H2O and decrease in osmolarity
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isotonic
proportional changes in sodium with changes in water
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hypotonic dilution or hypertonic concentration of extracellular fluid volume will?
cause water movement between ECF and ICF
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isotonic fluid deficit
causes: volume loss( vomiting and diarrhea), third spacing, endocrine disturbances

compensatory mechanisms: increased thirst, increased ADH

manifestations:

Vascular dehydration - decrease skin turgor, dry mucous membrane, sunken eyeballs

decrease vascular volume- postural hypotension, weak rapid pulse
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isotonic fluid volume excess
causes: decrease renal elimination (kidney disorder, heart and liver failure)

manifestations:

increased interstitial fluid volume: edema

increased vascular volume: bounding pulse, pulmonary edema ( shortness of breath, crackles, cough)
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dispropriate changes in sodium or oxygen leaves to what?
movement of oxygen between ICF and ECF
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hyponatremia
greater than 135

water moves into cells

manifestations: salt loss ( lethargy, anorexia, limp muscles, stupor)

treatment: add sodium via hypertonic IV solution, loop diuretic to increase oxygen elimination
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hypertonic translational
osmotic shift from ICF to ECF
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hypotonic dilution
sodium and water loss

edema
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hypernatremia
greater than 145

causes: water deficit, decreased oxygen intake, sodium administration

water moves out of cell

manifestations: dry skin, decrease tissue turgor, elevated body temperature

treatment: replacement fluids
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potassium
most intracellular electrolyte

essential for normal cell functions: osmolarity and fluid balance, glycogen and glucose deposition in skeletal muscle and liver, nerve and skeletal muscle and cardiac function

mechanisms of regulation: kidney and transcellular shift between ECF and ICF

3\.5-5.0
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renal regulation
ADH increases potassium which stimulates RAAS resulting in renal excretion

K+/H+ exchange
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extracellular-intracellular shifts
sodium/postassium-ATPase pump

potassium.hydrogen exchange

\
Insulin, catecholamines, and β-adrenergic agonists \n increase cellular uptake via ↑ Na+/K+-ATPase pump \n activity
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what is potassium vital to the regulation of?
resting membrane potential

opening sodium channels during action potential

rate of membrane repolarization

can have significant effects on cardiac, skeletal, and smooth muscle
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hyperkalemia
decreases membrane excitability
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hypokalemia
decreases resting membrane potential
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hypokalemia causes what?
inadequate intake

excessive losses- renal, skin, and GI

redistribution between ICF and ECF compartments

(diarrhea, insulin, eating disorders)
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hypokalemia manifestations
Impaired ability to concentrate urine – polyuria, polydipsia \n • GI – anorexia, N/V, constipation, abdominal distention, paralytic ileus \n • Neuromuscular – weakness, fatigue, muscle cramps, paresthesia, paralysis \n • Cardiovascular – postural hypotension, ECG changes, dysrhythmias \n • CNS – confusion, depression \n • Metabolic alkalosis
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hypokalemia treatment
IV replacement ( must be slow) (if not could cause cardiac arrest)
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hyperkalemia
causes: Decreased renal elimination – renal failure, Addison disease, K

\+-sparing diuretics, ACEi/ARBs \n • Excessive intake \n • Movement from ICF to ECF – tissue trauma, burns, seizures, acidosi
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hyperkalemia manifestations
GI –N/V/D, cramping \n • Neuromuscular – weakness, dizziness, muscle cramps, paresthesia \n • Cardiovascular –ECG changes, bradycardia, ventricular fibrillation, cardiac \n arrest
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hyperkalemia treatment
In emergent situations – IV insulin (plus glucose to prevent hypoglycemia), \n calcium, sodium bicarbonate \n • Insulin stimulates Na+/K+ pump – brings K+ into cells and pumps out Na+

\
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calcium
Normal level is 8.5 to 10.5 mg/dL. \n • Functions: \n • Bone strength and stability. \n • Membrane potentials and excitability. \n • Contraction of all muscle types. \n • Clotting. \n • Second messenger in many hormone and \n neurotransmitter pathways
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parathyroid hormone
Maintains blood calcium and phosphorous \n • Stimulates release of calcium and phosphorus \n from bone \n • ↑ renal resorption of calcium \n • ↑ GI calcium absorption \n • Requires activation of Vitamin D and magnesium \n • Vitamin D \n • Increases intestinal absorption of calcium \n phosphorous \n • Necessary for normal bone formation
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hypocalcemia
greater than 8.5

nerves fire more easily bc Calcium stabilizes neuromuscular excitability, making them less sensitive to stimuli

decrease in calcium and increases excitability

cardiovascular effects: hypotension and prolonged QT interval
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hypercalcemia
less than 10.5

Nerves are less able to fire → decreased excitability \n • Cardiovascular effects: hypertension, shortened QT interval
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phosphorus
normal 2.5-4.5

Functions: \n • Bone and ATP formation \n • Glucose, fat, protein metabolism \n • In DNA, RNA, phospholipids \n • Acid-base buffer \n • RBC, WBC, platelet function
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Magnesium
normal 1.3-2.1

Functions: \n • Cofactor in enzymatic reactions: \n • ATP generation \n • DNA replication \n • mRNA production and translation \n • Blocks K+ exit from cardiac cells \n • Smooth muscle relaxant