Flashcards in fluid and electrolytes Deck (110)
1
Na/K pump: what & how
what: active transporthow: Na out / K in
2
Na function x3
- skeletal + cardiac muscle contraction- nerve impulse transmission- water balance (where Na goes, H2O follows)
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* free H2O replenishment quantity calculation
[0.6 x wt (kg)]x[(measured Na/140) -1]
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individuals at risk for electrolyte abnormalities
- elderly- altered renal function- Acute/chronic renal disorders- Acute/chronic endocrine disorders- SIADH, DM- Mentally impaired- unable to access fluids- meds that alter fluid/electrolyte levels- all hospitalized patients
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thiazide diuretic site of action
distal convoluted tubule
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loop diuretic site of action
thick ascending limb
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aldosterone site of action
collecting duct
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hypernatremia is...
↓ H2O : Na in ECF = ↑ total body Na / ↓ total body H2O↓ intracellular fluid volume because H2O drawn out of cells
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acute water deficit rate of correction
1 mMol/hr
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chronic water deficit rate of correction
0.5 mMol/hr
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hypervolemic hypernatremia is
change in net body soluted/t...hypertonic saline or Na bicarb infusionskayexalate therapy (sodium polystyrene sulfonate)
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hypervolemic hypernatremia tx
diuretics w fluid replacement- free H2O- D5Wtreat the cause
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hypovolemic hypernatremia is
↓ body H2O + Nabut losing more *H2O*d/t...insufficient H2O intake: lt 600-700 ml/day loss of free H2O: excessive sweating, GI loss, osmotic diuresis
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hypovolemic hypernatremia tx
NS 0.9%- LOSING Na AND H2Omay need add’l fluids to meet needs: free H2O, D5W
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isovolemic hypernatremia is
↑Na, body H2O appropriated/t...inability to concentrate urineappropriate free H2O w/o Na excretion↑ serum osmolality (hyperglycemia, mannitol)
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isovolemic hypernatremia tx
diuretics w fluid replacement- free H2O- D5Wtreat the cause
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results of hypernatremia x4
↑ Na movement @ depolarization, = ↑ excitability/irritabilityH2O drawn osmotically out of cells = intracellular dehydration↓ intracellular fluid vol CNS: H2O shift brain interstitium → capillaries = cerebral atrophy
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hypernatremia: clinical signs
neuro- early: lethargy, weakness, irritability - later: twitching, seizures, coma, deathgeneral- dry/sticky mucosa- ↑ body temp (no fluid buffer for metabolic processes)- thirst
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hyponatremia is...
↑ H2O : Na in ECF = ↑ total body H2O ECF more dilute than ICF↓ excitable membrane depolarizationcellular swelling
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hyperosmolar hyponatremia is
↑ body concentration w ↓Na- ↑ intravascular oncotic P (hyperglycemia, mannitol)- ICF → extracellular space- ↓ TBW- altered urine Na excretion-- low - typical, Na retention appropriate---- d/t → extrarenal loss (GI, skin)-- normal/high---- d/t → renal loss (diuretic [thiazide], adrenal insufficiency, Na-losing nephropathy)
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hypoosmolar hyponatremia types x3
hypervolemichypovolemicisovolemic
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isosmolar hyponatremia is...
LESS COMMON usually d/t lab errorNa conc displaced w/o change in TBW contentmachine mistakes the following for electrolytes that don’t exist:- hyperlipidemia- hyperproteinemia- hyperglycemiafix apparent issues above before addressing Na (may be artifactual)
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isosmolar hyponatremia tx
determine urgency of replacement: acute onset, Na
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hypernatremia vs hyponatremia: difference between the types
hypernatremia: r/t volumehyponatremia: r/t osmolarity
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* altered urine excretion of Na in hyponatremia x2
low - typical, Na retention appropriate- low Na d/t → extrarenal loss (GI, skin)normal/high- low Na d/t → renal loss (diuretic [thiazide], adrenal insufficiency, Na-losing nephropathy)
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hypervolemic hypoosmolar hyponatremia
- see often d/t fluid dilution- ↑ hydrostatic P → peripheral edema, ascites, pulm edema- r/t ADH release from intravascular dehydration (CHF, cirrhosis, nephrotic syndrome, ARF or CRF)
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hypovolemic hypoosmolar hyponatremia
- presentation: dehydrated- intrinsic free H2O repletion exceeds Na repletion-- d/t renal: over-diuresis, adrenal insufficiency, cerebral Na-wasting syndrome-- d/t extrarenal: n/v, skin loss (ex: burn)
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isovolemic hypoosmolar hyponatremia
total body fluid normal w high ingestion lyte-deplete fluids- more common if excretion impaired- psychogenic polydipsia- beer potomania (beer-drinkers hyponatremia)- SIADH
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hyponatremia tx
- free H2O restriction (when appropriate; look @ volume status)- vasopressin V2 receptor antagonists (collecting ducts)- medical tx: aquaphoresis, slow continuous ultrafiltration (SCUF)- Na replacement: foods, IVF- hypertonic saline (3% NS) EXTREME CAUTION! can cause dramatic shift -- monitor rate, serial BMP q4-6 hours
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hyponatremia results
H2O osmotically drawn into cells: intracellular overhydration, cell lysis,;↑ ICF volume
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hypernatremia vs hyponatremia results
hyper: cell atrophy (water out)hypo: cell lysis (water in)
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hypovolemic hypoosmolar hyponatremia causes x2
renal: overdiuresis, adrenal insufficiency, cerebral salt wasting syndromeextrarenal: n/v, skin loss
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K function x6
H2O balancenerve impulse transmissiontissue synthesismuscle contractioncarb metabolismacid-base balance
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hyperkalemia is...
↑ extracellular K+↓ difference between ICF / ECF concentrationsfux up electrical neutrality- ↑ excitability- easy spontaneous stim / difficult appropriate stimulation
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hyperkalemia causes
- 2 much repletion- ↑ intake- renal dz (+ K replacement)- hypoaldosteronism- ACE inhibitors, ARBs- spironolactone (aldosterone antagonist)- RBC hemolysis- tumor lysis syndrome- acidosis (excess extracellular H+)-- body wants H+ → cell ∴ K+ → extracellular
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relationship between hyperkalemia and acidosis
acidosis = excess extracellular H = H → cell∴ K → ECF (balance)
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hyperkalemia clinical signs
NEUROneuralgias, paresthesias, weakness/paralysis, muscle twitchingGIn, d, intermittent colic↑ non specific / will kill you ↓CARDIAC- ↓ RMP- ↓ relative refractory period- peaked T waves- prolonged QRS,- ↓ P wave- sine wave, v fib, asystoleearly: excitable / late: 2 much K = slower conduction (Na open slow)!! often asymptomatic until cardiac arrest !!
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lyte imbalance often asymptomatic until cardiac arrest
hyperkalemia
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hyperkalemia tx
FIND THE CAUSE ASAPsymptomatic = intervene faster!!- restrict intake / potentiating rx- promote → cell-- IV Insulin w 50% Dextrose (D50) -- albuterol- remove from body-- dialysis (HD or PD)-- PD only if already on - don’t initiate-- emergent dialysis if K ↑↑↑-- kayexalate (Na for K in gut)- stabilize membrane action potential- Ca (Chloride/Gluconate/Carbonate)-- CaCl = 3x available Ca vs gluconate + CENTRAL LINE -- CaCarb = PO- Na bicarb (shifts acid-base bal so K back in)
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hyperkalemia tx: promote K+ → cell x2
IV insulin w D50- dex 4 hypoglycemia, preventionalbuterol- can power Na/K pumps
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hyperkalemia: stabilize membrane action potential x3
Ca (Chloride/Gluconate/Carbonate)- ↑ threshold potential; re-establishes gap btw resting + threshold. TEMPORARY FIX!-- CaCl = 3x available Ca vs gluconate + CENTRAL LINE --CaCarb = PONa bicarb (shifts acid-base bal so K back in)
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hypokalemia is
- ↓ extracellular K+- ↑ difference btw ICF + ECF concentrations-- ↓ excitability of cellsK+ ↓ ICF + ECF
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hypokalemia causes
- ↓ intake, malnutrition- hyperaldosteronism- rx induced: diuretics hyperinsulinism, hyperalimentation- v, gastric suction- alkalosis- contraction alkalosis
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hypokalemia s/s
MUSCULARskeletal weakness ↓DTRsNEUROirritability, confusion, lethargyGI smooth muscle weakness↓peristalsis/paralytic ileusCARDIACmore neg RMP↑ relative refractory periodEKG change d/t K hanging out- non‐specific ST changes- T wave flattening / inversion- U wave- sinus brady- arrhythmias (esp vent)- PVC = myocard irritated bc can't be stim'd
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hypokalemia tx
ABOVE ALL: FIND CAUSE- PO supplements- diet- change diuretic-- spironolactone -- eplerenone (Inspra)-- amiloride (Midamor)IV repletion (only if symptomatic)maybe Mg repletion
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alkalosis and hypokalemia relationship
↓ H in ECF = H in ICF → ECF to buffer excess bicarbK → ICF (maintain electroneutrality) = serum K ↓- contraction alkalosi
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insufficient H2O intake #
less than 600 - 700 mL/day
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contraction alkalosis + hypokalemia
loss K d/t loss body fluid not containing bicarb- aka -↑ blood pH d/t fluid lossseen w: diuretic tx- CHF- renal failure- ↑↑ loop diuretics = pee K out = Na + H → cell = BICARB LEFT BEHIND-- even w K replacement, H + Na still shift = alkalotic- iatrogenic- GI losses
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when is IV K appropriate for hypokalemia
symptomatic only!
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Mg #s
1.5 - 2.6
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Mg critical for
skeletal muscle contraction, carb metabolism, ATP formation, vitamin activation, cellular growth
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hyper vs hypo mag
hyper: ↓ membrane excitabilityhypo: ↑ membrane excitability
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hypermag causes
↑ intake- antacids- laxatives- excessive Mg2+ replacement↓ renal function
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hypomag causes
↓ intake -OR- ↑ loss- malnutrition/starvation- EtOH ingestion- upper GI loss, d/steatorrhea, malabs conditions-- ex: bariatric surgery, celiac, ulcerative colitis- rx interactions: diuretics, aminoglycosides, amphotericin B
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rx interactions leading to hypomag
etics, aminoglycosides, amphotericin B
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hypermag s/s
EKG similar to hyperK, better toleratedovert s/s at gt 4.0CV- brady- periph vasodilation- hypotension- prolonged PRI- widened QRS- ↓ diastolic BPCNS- ↓ nerve impulse transmission- drowsy/lethargicNEURO- ↓ DTRs- progressively weaker skel musc contractions
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hypomag s/s
VERY VERY IRRITABLENEURO- hyperactive DTRs- paresthesias - muscle spasms @ rest CNS- psych depression- psychosis- confusionGI - paralytic ileus- n/v- anorexia/constipation
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hypermag tx
mimic hyperkalemia tx- insulin/D50/IVF- d/c supplementation- loopsdialysisprevention (cautious repletion) body tends to tolerate / manage mag well on its own
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body tends to tolerate/manage which lyte imbalance well on its own?
magnesium
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hypomag tx
FIND CAUSE (iatrogenic?)d/c pharm contribspharm repletionMg Gluconate or ChlorideMg Sulfate IVMg Oxide (NOT Hydroxide ← laxative!!)
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Ca2+ #s
9 - 10.5 mg/dL -- BOUND4.5 - 5.6 (free/ionized)
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hypercalcemia is...
- ↑ serum Ca- dysfxnal control mechanism- excitable tissues less sensitive to stim: heart, skeletal, & smooth muscles, nerves-- takes less stimuli to contract ∴ cells not as responsive- ↓ clotting time (faster clot)- kidney stones (d/t attempt to excrete)
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hypocalcemia is...
- ↓ serum concentrations- ↑ Na across membranes- ↑ membrane excitability- depolarizations easier & inappropriate
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hypercalcemia causes
- ↑ intake (milk‐alkali syndrome)- vit D toxicity (↑D3 = ↑ gut abs)- immobility- hyperparathyroidism- malignancies (tumor lysis syndrome)- rx: thiazides, glucocorticoids
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what is required for gut absorption of Ca
Vit D3
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rx causes of hypercalcemia
thiazidesglucocorticoids
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hypocalcemia causes
- ↓ intake/malnutrition- vit D deficiency- hypoparathyroid- hyperphosphatemia- EtOH abuse- citrate (anticoag in RBC transfusions)- pancreatitis- bicarb infusion- sepsis
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hypercalcemia s/s
neuro: AMS/lethargy/coma, muscle weakness, ↓ DTRsGI: constipation, paralytic ileus, anorexia, n/vheme: ↑ clotting (DVTs)behavioral: mild change to psychosisrenal: polyuria, polydipsiaCV: tachycardia → bradycardia“tachy-brady syndrome", htn (↑ vascular tone)
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tachy brady syndrome assoc with which lyte abnormality
hypercalcemia
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hypocalcemia s/s
neuro: paresthesias peripherally (pins & needles), facial twitching/tingling, trousseau's sign, chvostek's signCV: brady, hypo, prolonged ST & QTGI: ↑ peristalsis, abd spasms, diarrheaMS: muscle spasm @ rest, osteoporosis, hyperactive DTRs
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trousseau's sign
BP cuff inflation = twitchy twitchyassoc with hypoca
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chvostek's sign
poke cheeky = twitchy twitchyassoc with hypoca
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hyperca tx
d/c: LR, Ca2+ & vit D supplements (MVI/antacids), thiazide diuretics0.9% sodium chloride & loop sglucocorticoids (cause & tx; bone demineralization or suspends Ca in blood to excrete)prostaglandin synthesis inhibitors (NSAIDS)bisphosphates ⊣ bone resorption (Pamidronate, Etidronate) Ca binders (Plicamycin, Penicillamine)PO4 salts (last resort - Ca/PO4 balance)- K‐phos- Neutra‐phosHD
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this lyte imbalance needs adjustment for hypoalbuminemia
hypocalcemia
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hypocalcemia tx
nutritional support: dairy, green leafy vegetables, nuts, fishreplacement- PO: Caltrate/Oscale, Ca carbonate- IV: Ca Gluconate (central not req but could necrose), Ca Chloride - CENTRAL LINE!
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Ca replacement requiring central line
CALCIUM CHLORIDE
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PTH actions: effect, bone, gut, kidney
effect: ↑ Ca ↓ PO4bone: ↑ osteoclastsgut: indirect via vit Dkidney: Ca in PO4 out
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Vit D3: effect, bone, gut, kidney
effect: ↑ Ca ↑PO4bone: nonegut: ↑ Ca ↑PO4kidney: none
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serum bicarb + kidneys relationship
HCO3 takes time to change! high level = chronic acidosis causing bicarb to be retained in response
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BMP CO2 tells us what
it's equivalent to HCO3 ABG BUT it is CO2 in serum NOT in gas (that's ABG)
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THIS LYTE TAKES TIME TO CHANGE!!!!
HCO3 via kidneys
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elevated bicarb causes
metabolic alkalosisprimary ingestion (ex: tums for heart burn)iatrogenic: over‐replacementcontraction alkalosis (volume depletion)metabolic response to respiratory acidosis- poss norm for chronic COPDer- sometimes tolerated given PMH DON'T JUST TX OUT OF RANGE #
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contraction alkalosis and volume relationship
volume CONTRACTION (depletion) hence the name!
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elevated bicarb tx
FIND CAUSEadjust pharmmaximize renal perfusion (consider supplementation if kidneys screwy)
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low bicarb causes
non‐gap (hyperchloremic): 8-16 = normal range ← d/t lossrenal tubular acidosisdiarrhea (bicarbonate loss)urinary diversionsgap 16+ (low bicarb or retaining H)MUDPILESMethanolUremiaDiabetic ketoacidosisPropylene glycol (in IV ativan, fireball)IsoniazidLactic acidosisEthylene glycol (antifreeze, radiator moonshine)Salicylates
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** MUDPILES
gap acidosis (16+)M ethanolU remiaD KAP ropylene glycol I soniazidL actic acidosisE thylene glycol S alicylates
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elevated BUN causes
aka azotemiaAKICKDpre‐renal state (CHF, shock, hypovolemia)hypercatabolic state/steroidsupper GI bleedhigh protein feedingaggressive diuretic tx
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elevated BUN aka
azotemia
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low BUN... wtf?!
causes...younger agemalnourishedhemodilutionhepatic failure tx: given cause, is intervention really necessary?
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elevated BUN s/s
NEUROMUSCULAR- AMS- coma- encephalopathy- fatigue/weakness- myalgias- neuropathy- seizuresGIanorexia, nauseaGUamenorrhea, sexual dysfxnMISCaltered taste/smellsleep disturbancesuremic frost (N excreted via skin)
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uremic frost
N excreted via skin r/t elevated BUN
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elevated BUN tx
ID THE DAMN CAUSE- pathologic?- GI bleed, over diuresis, hyperalimentation?- pharmacologic?
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what is creatinine
catabolic byproduct of creatine phosphatereleased from muscle @ constant ratefiltered through kidneys (waste product) @ constant rateGFR marker
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what does a rise in creatinine indicate?
kidneys are excreting out less - GFR MARKER!DOES NOT MEAN MORE MADE
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elevated creat causes
impaired renal fxn: AKI, CKD
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low creat causes
muscle wasting ∴ mass loss- liver disease- malnutritionpregnancy
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elevated creat s/s
low‐grade feverfatigue/lethargy/malaiseanorexia, weight changedehydrationheadachedyspneamental status changes (encephalopathy)
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elevated creat tx
↓ production not possibleDETERMINE CAUSEdialysis: look at patient’s clinical picture to decide when
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how to tell if renal fxnal level appropriate?
1. is creatinine appropriate?2. compare to BUNgreater than 20 = prerenal failureless than 10:1 = intrarenal failure10 - 20:1 =- normal - if ↑ creat + proportional BUN, post-renal failure
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phosphate #s
3 to 4.5 mg/dL
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dietary phosphate
red meat, fish, poultry, eggs, milk, whole grains, nuts, legumes ; cola beverages ; prepackaged fast foods; preservatives
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hyperphosphatemia is
greater than 4.5 mg/dLTYPICALLY WELL TOLERATEDeffects d/t hypocalcemia
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hyperphosphatemia s/s
hypocalcemia!neuro: paresthesias peripherally (pins & needles), facial twitching/tingling, trousseau's sign, chvostek's signCV: brady, hypo, prolonged ST & QTGI: ↑ peristalsis, abd spasms, diarrheaMS: muscle spasm @ rest, osteoporosis, hyperactive DTRs
104
hyperphosphatemia tx
dietary restrictions: soft drinks super badoral phosphate binders- Phoslo (Calcium Acetate)- Renagel (Sevelamer)- Alucaps (Aluminum Hydroxide‐ base for antacids)***MUST BE GIVEN WITH FOOD***-- these don't pull phosphate out of blood!IVF in severe cases
105
hypophosphatemia causes
- malnutrition/starvation- Mg & Al-based antacids- excessive phosphate binder - hyperparathyroidism- hyperalimentation (PO/PT/IV)- renal failure- EtOH abuse (lytes depleted)
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hypophosphatemia s/s
hypercalcemia!
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phosphate and calcium
BALANCE ∴ INVERSE RELATIONSHIP!hypocalcemia = hyperphosphatemiahypercalcemia = hypophosphatemia
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hypophosphatemia tx
dietary repletionpharmacologic repletion- PO/PT: K‐Phos/Neutra‐Phos- IV: Na Phosphate/K Phosphate-- pay attention to Na and K levels!CAUTION with IV repletion- do not exceed 7 mmol/hr- K+ /Na+ supplementation
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** hypophosphatemia: caution with IV repletion **
- do not exceed 7 mmol/hr- K+ /Na+ supplementation
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