Fluid and Electrolyte imbalances Flashcards
causes of extracellular edema
- increased capillary hydrostatic pressure
- decreased plasma proteins
- increased capillary permeability
- blockage of lymph return
factors that can increase capillary hydrostatic pressure
- excess kidney retention of salt and water (acute/chronic KI, mineralocorticoid excess)
- high venous pressure ( HF, venous obstruction, failure of venous pumps)
- decreased arteriolar resistance (excessive body heat, insufficiency of SNS, vasodilator drugs)
factors that can decrease plasma protein concentration
loss of protein in urine (nephrotic syndrome)
loss of proteins from denuded skin areas (burns/wounds)
failure to produce . proteins (such as in liver dz or severe protein or caloric malnutrition)
factors that can increase capillary permeability
immune rxns that cause release of histamine toxins bacterial infections vit deficiency (esp. c) prolonged ischemia burns
factors that can block lymph return
cancer
infections (filarial, nematodes )
surgery
congenital absence or abnormality of lymphatic vessels
factors working to prevent extracellular edema from occurring
interstitium normally has a low compliance
lymph flow has a capacitance to increase 10-50 fold
increased amounts of protein-poor capillary fluid flow wash proteins out from the interstitial space, thereby decreasing net capillary filtration pressure
causes of intracellular edema
- depression of metabolic systems of tissue
- lack of adequate nutrition to the cells
cells lack the resources to drive the NA/K ATPase so na accumulates in cells and they expand (water follows Na into cells) - too little extracellular Na
- too much water
increased RBF and GFR leads to
increased delivery of oslute to JG apparatus (senseed by macula densa )
increased resistance of afferent arterioles
decreased RBF, GFR
ECV sensors
low pressure . - cardiac atria and pulmonary vasculature
high pressure - carotid sinus, aortic arch, JG apparatus of kidney
regulatory hormones of the proximal tubule
angiotensin II, noreepinephrine and epinephrine
regulatory hormones of hte late distal tubuel and collecting ducts
aldosterone, atrial natriuretic peptide
increased Na intake leads to \_\_\_\_ ECF AND EABV \_\_\_\_ sympathetics \_\_\_\_\_ ANP \_\_\_\_\_\_ PIc \_\_\_\_\_\_ RAAS
increased ECF volume and increased effective arterial blood volume decreasing sympathetic (dilaiton of afferent arterioles, decreased na reabsorption in PT), increasing ANP (constricting efferent arterioles, decreased Na reabsorption) decreaseing PIc, decreased RAAS
clinical signs of hypovolemia
decreased skin turgor 9tenting) thirst dry mucous membranes sunken eyes oliguria progressing to tachycardia, hypotension, tachypnea, confusion
clinical signs of hypervolemia
weight gain
edema
bounding pulse
causes of absolute hypovolemia
extra-renal - bleeding, GI fluid loss, skin fluid loss, respiratory fluid loss, extracorproreal ultrafiltration
renal - diuretics, na wasting tubulopathies, genetic or acquired tubulointerstitial disease, obstructive uropathy/postobstructive diuresis, hormone deficiency, hypoaldosteronism adrenal insufficiency
causes of relative hypovolemia
extrarenal - edmatous states, HF, cirrhosis, anaphylaxis, drugs, spesis, pregnancy, third space loss
renal - severe nephrotic syndrome
causes of volume excess
primary renal na retention (increased effective circulating volume) d/t - oliguric acute renal failure acute glomerulonephritis sevrere chronic renal failure nephritic, nephrotic syndrome primary hyperaldsoteronism cushing syndrome early stages of severe liver dz conn syndrome gorndon syndrome liddle syndrome secondary renal Na retention (decreased ECV) HF, later stages of severe liver dz, nephrotic syn drome, pregnancy
hyper/hyponatremia is a problem with
WATER
hypo <135
hyper >145
normal plasma osmolality value
285-295
quick estimate = 2x [Na]
vasopressin is more responsive to changes in blood pressure or plasma osmolality
plasma osmolality
factors that increase the secretion of ADH
increased plasma osmolality decreased blood volume decreased blood pressure nausea/hypoxia drugs: mrophine, nicotine, cyclophosphamide
factors that decrease the secretion of ADH
decreased plasma osmolarity
increased blood volume
increased blood pressure
drugs: alcohol clonidine haloperidol
factors that increase thirst
increased osmolarity decreased blood volume decreased blood pressure increased angiotensin II dryness of mouth
factors that decrease thirst
decreased osmolarity increased blood volume icnreased blood pressure decreased angiotensin II gastric distension
effect of diarrhea on body fluid compartments
loss of osmotic ECF only
effect of water deprivation on body fluid compartments
loss of h2o from icf and ecf
increased osmolarity in both compartments
effect of adrenal insufficiency on body fluid compartments
lost na
increased volume icf
decreased ecf
both vbecome hypo-osmotic
plasma sodium concentration of less than 135 meq/l
hyponatremia
symptoms of hyponatremia and pneumonic
SALT LOSS stupor/coma anorexia, n/v lethargy tendon reflexes decreased
limp muscles
orthostatic hypotensin
seizures/HA
stomach cramping
tx of hyponatremia
level 3 - severe - hypertonic NaCl followed by fluid restriction
level 2 - moderate - vaptan or hypertonic nacl
level 1 - fluid restriction
rapid overcorrection of hyponatremia can lead to
osmotic demyelination syndrome
things that can cause SIADH
tumors producing vasopressin ectopically drug induced brain tumors idiopathic subarachnoid hemorrhage stroke inflammatory brain lesions respiratoyr fialure HIV traumatic brain injury drug induced pneumonia neusea, pain, prolonged exercise post op
scenarios where hypernatremia is suspectedd
living alone who fall at home
indicator of neglect in nursing homes
in the desert without enough water
major causes of jhypernatremia
unreplaced water loss in scenarious such as sweat, gi losses, central/nephrogenic diabetes insipidus, osmotic diuresis or hypothalamic lesions
water loss into cells - sever exercise or seizures
sodium overload - ate too much salt
mneumonic of hypernatremia
TRIP twitching, tremors, hyperreflexia restlessness, irritability, oncfusion intestine thirst, dry mouth, decreased urine output pulmonary and peripheral edema
hyperkale is plasma concentration above
5.2
hypokalemia is plasma concentration below
3.7
hypokalemia does what to the plasma membrane of cells
HYPER-polarizes it - less likely to fire
but in cardiac tissue it causes tachycardia
hyperkalemia does what to plasma membrane threshold
decreases it hypopolarizes more likely to fire lethal kcl injection messes up membrane potential in cardiac tissue become HYPERPOLARIZED
effet of hyperkalemia on EKG
high t wave
effect of hypokalemia on ECG
low t wave, high u wave, low ST segment in severe hypokalemia
things that induce potassium uptake into cells
INSULIN ALKALEMIA (buffering mechanism) b2 agonist, aldsoterone deficiency, alpha blockers, alkalosis, hypoosmolarity
things that induce potassium eflux from cells
alpha agonist insulin deficiency aldosterone b2 blockers ACIDOSIS (buffering) hyperosmolarity exercise cell lysis
aldosterone effects what cells in the glomerulus
principal cells in the collecting ducts
high na intake increases/decreases/does not influence k excretion
does not influence decreased aldosterone (decreasing secretion) from na intake is offset by increased GFR and decreasd proximal tubular na reabosrption
hypokalemia causes mneumonic
graphic idea GI losses (vomitting, diarrhea) renal tubular acidosis (1 and 2 types) aldosterone paralysis hypothermia insulin excess cushing syndrome
insufficient intake
diuretics
elevated beta adrenergic activity
alkalosis
signs and symptoms of hypokalemia
CNS - drowsiness, letahrgy
neuromuscular *** - skeletal muscle weakness, smooth msucle weakness leading to ileus and constipation
cardiovascular - ventricular arrhythmias, hypotension, cardiac arrest
renal - impaired concentrating ability causes polyuria and nocturia
metabolic - hyperglycemia
causes of hyperkalemia mneumonic
RED FETS
renal disease - arf, ckd, type IV RTA .
excessive intake - food, k iv fluids, blood transfusion
drugs - k sparing diuretics, k salts of penicillin
factitious: pro0longed use of tourniquet, hemolysis
endocrineL addisons disease
tissue release: rhabdomyolysis, burns, hemolysis, cytotoxic therapy
shift out of cell - acidosis, beta antagonsit, insulin deficiency, tissue damage
signs and symptoms of hyperkalemia
cardiac - abnromal heat rhythm, bradycardia
peaked t wave
neuromuscular - numbness, weakness, flaccid paralysis
drug causes of hyperkalemia
drugs targeting RAAS
