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Total Body Water
body fluids compose 60% of total body weight
2/3rd of the body H2O is in the ICF
1/3rd of the body H2O is in the ECF
affected by gender and age (decrease as we age)
Interstitial fluid and plasma
nearly identical because they care constantly mixing
Edema
excess retention of interstitial fluid resulting in swelling
can be anywhere but most noticeable in extremeities
localized - due to trauma or around an organ
generalized - uniform distribution of fluid
Capillary Hydrostatic Pressure (CHP)
pushes fluid out of capillary (BP)
Capillary Osmotic Pressure (COP)
pulls fluid into capillary (albumin)
Interstitial Fluid Hydrostatic Pressure (IFHP)
pushes fluid into capillary
Interstitial Fluid Osmotic Pressure (IFOP)
pulls fluid into interstitial space
Causes of Edema
increased capillary filtration
decreased capillary reabsorption
increased capillary permeability (caused by histamine, allows leakage)
lymphatic obstruction
Net filtration
(CHP + IFOP) - (IFHP + COP)
Consequences of Edema
tissue necrosis
oxygen delivery and waste removal imparied
pulmonary edem
hypoxia
cerebral edema
headaches, nausea, seizures, coma, death
circulatory shock
excess fluid in tissue spaces causes low blood volume and low BP
Left Heart Failure
inability of left side to pump into systemic circulation
congestion in lungs
pulmonary edema
Right Heart Failure
inability of right side to adequately pump venous blood into pulmonary circulation
congestion in the body
pitting edema, ascites
Ascites
accumulation of fluid in peritoneal space
MCC: liver cirrhosis → portal hypertension
pathophysiology - decrease albumin, decreased cop, edema
Lymphedema
localized edema
accumulation of lymphatic fluid
often due to lymph node removal
Decreased water loss leads to
increased blood volume
Anti-diuretic hormone
decrease water loss due to H2O reabsorption in the kidney
Aldosterone
renal reabsorb sodium (H2O follow)
excrete potassium
ANP and BNP stimulate
renal elimination of Sodium (H2O follows Na+)
What triggers release of ANP and BNP
increase blood volume/blood pressure
What effect does the release of ANP and BNP have
decrease sodium
decrease blood volume
decrease blood pressure
Hypovolemia
decrease blood volume
hypervolemia
increase blood volume
Kidney releases renin when it detects
decreased blood volume
decreased blood pressure
decrease sodium
effect of kidney releasing renin
increase ADH (vasopressin)
increased thirst → increased blood volume
sympathetic nervous system
vasoconstriction → increased blood pressure
increase aldosterone
ADH / Vasopressin
made in hypothalamus
stored in posterior pituitary
targets DCT and CD in the kidney
reabsorbs H2O back into circulation
What triggers release of ADH
increase osmolarity
decrease BV/ decreased BP
Hypernatremia
increase sodium
decreased water intake
increased water loss
diuretics, vomiting, diarrhea
sweating, dehydration
hyper secretion of aldosterone
Diabetes insipidus
Hyponatremia
decrease sodium
increased water intake
water intoxication
diuretics, vomiting, diarrhea
SIADH
kidney, heart, liver dysfunction
Syndrome of Inappropriate ADH Secretion (SIADH)
increase ADH
hyponatremia
causes: idiopathic, brain trauma, paraneoplastic syndrome, Medication SE
pathophysiology
increased H2O Reabsorption → decreased sodium
decreased serum osmolarity
increased urine osmolarity
decreased urine volume
“Water intoxication”
Paraneoplastic Syndrome
the consequence of cancer in the body, but unlike mass effect, is not due to the local presence of cancer cells
most common types
humoral hypercalcemia of malignancy in squamous cell carcinoma
syndrome of inappropriate antidiuretic hormone in small cell lung cancer
Diabetes Insipidus
insufficiency of ADH
Cause of Neurogenic Diabetes Insipidus
absence of ADH
pituitary problem such as brain tumor, hypophysectomy, aneurysm, thrombus, infection
result of TBI
Cause of Nephrogenic diabetes insipidus
inadequate response of renal tubules to ADH
Pyelonephritis, PKD, amyloidosis
Meds - Lithium, Colchicine, Amphotericitin B, loop diuretics, general anesthetics
Gestational Diabetes Insipidus
increase levels of vasopressinase
ADH gets broken down
rare and usually no treatment necessary
Signs and Symptoms of Diabetes Insipidus
excessive urination and thirst
polyuria and polydipsia
excretion of large volume dilute urine, dehydration → 8-12 L/day vs 1-2 L/day (normal)
Testing for Diabetes Insipidus
increased serum osmolarity vs decreased urine osmolarity
plasma ADH levels
CT scan
Dehydration
s/s : hypotension and tachycardia
diagnosis
decreased skin turgor
decreased urine output
increased urine osmolarity
blood
increased HCT
increased serum osmolarity
increased BUN: Cr ration
treatment
PO rehydration
IV rehydration
Sodium
major cation outside of the cell (90%)
136-145 mEq/L
maintains ECF osmotic balance - water follows salt
function
maintain tonicity of ECF
facilitate nerve conduction and glandular secretions
Organs and hormones involved
kidney
aldosterone, ANP/BNP
most often goes hand in hand with chloride
Osmolality
concentration of stuff in the blood
Hypertonic solution
concentrated blood
Na: H2O ratio is high
hypernatremia
decreased water intake increased water loss
Hypotonic Solution
dilute blood
Na : H2O ratio is low
hyponatremia
increased water intake or decreased water loss
SIADH
signs and symptoms of hyponatremia
headache, lethargy
N/;V
confusion, disorientation
seizures, come
muscle weakness, cramps
hyporeflexia
signs and symptoms of hypernatremia
headache, restlessness
N/V, thirsty, tachycardia
confusion, disorientation
seizures, come
muscle twitching, spasms
hyperreflexia
Potassium (K+)
major cation inside of the cell (98%)
greatest contributor to intracellular osmosis and cell volume
plays a role in blood pH by affecting the plasma concentration
Hypokalemia
reduced intake of potassium
increased entry of potassium into cells
alkalosis
increased entry of body potassium
diarrhea, vomiting
Hyperkalemia
increased intake of potassium
acidosis
increased exit of potassium from cells
decreased renal excretion of potassium
Hypokalemia s/s and EKG
muscle weakness, cramps
depressed/flattened t waves
prominent U wave
Hyperkalemia s/s and EKG
muscle weakness, spasticity
wide QRS w/ tall peaked T waves
Calcitriol
activated in the kidney
increased Ca2+ absorption in GI
increased Ca2+ reabsorption in kidney
Hypocalcemia
parathyroid hormone
easier for Na+ to enter the cell
increased excitability
hyperreflexia
convulsions/seizures
Long QT interval
Hypercalcemia
hyperparathyroidism
short ST segment
decrease Na+ entry into cell
decreased excitability
Acidosis
hyperkalemia
hypercalcemia
decreased excitability of CNS
Alkalosis
over excitability of the CNS
hypokalemia
hypocalcemia