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monster management > fluid and electrolytes > Flashcards

fluid and electrolytes Flashcards

1
Q

Na/K pump: what & how

A

what: active transporthow: Na out / K in

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2
Q

Na function x3

A
  • skeletal + cardiac muscle contraction- nerve impulse transmission- water balance (where Na goes, H2O follows)
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3
Q
  • free H2O replenishment quantity calculation
A

[0.6 x wt (kg)]x[(measured Na/140) -1]

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4
Q

individuals at risk for electrolyte abnormalities

A
  • 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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5
Q

thiazide diuretic site of action

A

distal convoluted tubule

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6
Q

loop diuretic site of action

A

thick ascending limb

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7
Q

aldosterone site of action

A

collecting duct

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8
Q

hypernatremia is…

A

↓ H2O : Na in ECF = ↑ total body Na / ↓ total body H2O↓ intracellular fluid volume because H2O drawn out of cells

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9
Q

acute water deficit rate of correction

A

1 mMol/hr

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10
Q

chronic water deficit rate of correction

A

0.5 mMol/hr

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11
Q

hypervolemic hypernatremia is

A

change in net body soluted/t…hypertonic saline or Na bicarb infusionskayexalate therapy (sodium polystyrene sulfonate)

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12
Q

hypervolemic hypernatremia tx

A

diuretics w fluid replacement- free H2O- D5Wtreat the cause

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13
Q

hypovolemic hypernatremia is

A

↓ body H2O + Nabut losing more H2Od/t…insufficient H2O intake: lt 600-700 ml/day loss of free H2O: excessive sweating, GI loss, osmotic diuresis

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14
Q

hypovolemic hypernatremia tx

A

NS 0.9%- LOSING Na AND H2Omay need add’l fluids to meet needs: free H2O, D5W

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15
Q

isovolemic hypernatremia is

A

↑Na, body H2O appropriated/t…inability to concentrate urineappropriate free H2O w/o Na excretion↑ serum osmolality (hyperglycemia, mannitol)

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16
Q

isovolemic hypernatremia tx

A

diuretics w fluid replacement- free H2O- D5Wtreat the cause

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17
Q

results of hypernatremia x4

A

↑ 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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18
Q

hypernatremia: clinical signs

A

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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19
Q

hyponatremia is…

A

↑ H2O : Na in ECF = ↑ total body H2O ECF more dilute than ICF↓ excitable membrane depolarizationcellular swelling

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20
Q

hyperosmolar hyponatremia is

A

↑ 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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21
Q

hypoosmolar hyponatremia types x3

A

hypervolemichypovolemicisovolemic

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22
Q

isosmolar hyponatremia is…

A

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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23
Q

isosmolar hyponatremia tx

A

determine urgency of replacement: acute onset, Na

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24
Q

hypernatremia vs hyponatremia: difference between the types

A

hypernatremia: r/t volumehyponatremia: r/t osmolarity

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25
Q
  • altered urine excretion of Na in hyponatremia x2
A

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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26
Q

hypervolemic hypoosmolar hyponatremia

A
  • 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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27
Q

hypovolemic hypoosmolar hyponatremia

A
  • 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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28
Q

isovolemic hypoosmolar hyponatremia

A

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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29
Q

hyponatremia tx

A
  • 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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30
Q

hyponatremia results

A

H2O osmotically drawn into cells: intracellular overhydration, cell lysis,;↑ ICF volume

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31
Q

hypernatremia vs hyponatremia results

A

hyper: cell atrophy (water out)hypo: cell lysis (water in)

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32
Q

hypovolemic hypoosmolar hyponatremia causes x2

A

renal: overdiuresis, adrenal insufficiency, cerebral salt wasting syndromeextrarenal: n/v, skin loss

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33
Q

K function x6

A

H2O balancenerve impulse transmissiontissue synthesismuscle contractioncarb metabolismacid-base balance

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34
Q

hyperkalemia is…

A

↑ extracellular K+↓ difference between ICF / ECF concentrationsfux up electrical neutrality- ↑ excitability- easy spontaneous stim / difficult appropriate stimulation

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35
Q

hyperkalemia causes

A
  • 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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36
Q

relationship between hyperkalemia and acidosis

A

acidosis = excess extracellular H = H → cell∴ K → ECF (balance)

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37
Q

hyperkalemia clinical signs

A

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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38
Q

lyte imbalance often asymptomatic until cardiac arrest

A

hyperkalemia

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39
Q

hyperkalemia tx

A

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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40
Q

hyperkalemia tx: promote K+ → cell x2

A

IV insulin w D50- dex 4 hypoglycemia, preventionalbuterol- can power Na/K pumps

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41
Q

hyperkalemia: stabilize membrane action potential x3

A

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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42
Q

hypokalemia is

A
  • ↓ extracellular K+- ↑ difference btw ICF + ECF concentrations– ↓ excitability of cellsK+ ↓ ICF + ECF
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43
Q

hypokalemia causes

A
  • ↓ intake, malnutrition- hyperaldosteronism- rx induced: diuretics hyperinsulinism, hyperalimentation- v, gastric suction- alkalosis- contraction alkalosis
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44
Q

hypokalemia s/s

A

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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45
Q

hypokalemia tx

A

ABOVE ALL: FIND CAUSE- PO supplements- diet- change diuretic– spironolactone – eplerenone (Inspra)– amiloride (Midamor)IV repletion (only if symptomatic)maybe Mg repletion

46
Q

alkalosis and hypokalemia relationship

A

↓ H in ECF = H in ICF → ECF to buffer excess bicarbK → ICF (maintain electroneutrality) = serum K ↓- contraction alkalosi

47
Q

insufficient H2O intake #

A

less than 600 - 700 mL/day

48
Q

contraction alkalosis + hypokalemia

A

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

49
Q

when is IV K appropriate for hypokalemia

A

symptomatic only!

50
Q

Mg #s

A

1.5 - 2.6

51
Q

Mg critical for

A

skeletal muscle contraction, carb metabolism, ATP formation, vitamin activation, cellular growth

52
Q

hyper vs hypo mag

A

hyper: ↓ membrane excitabilityhypo: ↑ membrane excitability

53
Q

hypermag causes

A

↑ intake- antacids- laxatives- excessive Mg2+ replacement↓ renal function

54
Q

hypomag causes

A

↓ 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

55
Q

rx interactions leading to hypomag

A

etics, aminoglycosides, amphotericin B

56
Q

hypermag s/s

A

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

57
Q

hypomag s/s

A

VERY VERY IRRITABLENEURO- hyperactive DTRs- paresthesias - muscle spasms @ rest CNS- psych depression- psychosis- confusionGI - paralytic ileus- n/v- anorexia/constipation

58
Q

hypermag tx

A

mimic hyperkalemia tx- insulin/D50/IVF- d/c supplementation- loopsdialysisprevention (cautious repletion) body tends to tolerate / manage mag well on its own

59
Q

body tends to tolerate/manage which lyte imbalance well on its own?

A

magnesium

60
Q

hypomag tx

A

FIND CAUSE (iatrogenic?)d/c pharm contribspharm repletionMg Gluconate or ChlorideMg Sulfate IVMg Oxide (NOT Hydroxide ← laxative!!)

61
Q

Ca2+ #s

A

9 - 10.5 mg/dL – BOUND4.5 - 5.6 (free/ionized)

62
Q

hypercalcemia is…

A
  • ↑ 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)
63
Q

hypocalcemia is…

A
  • ↓ serum concentrations- ↑ Na across membranes- ↑ membrane excitability- depolarizations easier & inappropriate
64
Q

hypercalcemia causes

A
  • ↑ intake (milk‐alkali syndrome)- vit D toxicity (↑D3 = ↑ gut abs)- immobility- hyperparathyroidism- malignancies (tumor lysis syndrome)- rx: thiazides, glucocorticoids
65
Q

what is required for gut absorption of Ca

A

Vit D3

66
Q

rx causes of hypercalcemia

A

thiazidesglucocorticoids

67
Q

hypocalcemia causes

A
  • ↓ intake/malnutrition- vit D deficiency- hypoparathyroid- hyperphosphatemia- EtOH abuse- citrate (anticoag in RBC transfusions)- pancreatitis- bicarb infusion- sepsis
68
Q

hypercalcemia s/s

A

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)

69
Q

tachy brady syndrome assoc with which lyte abnormality

A

hypercalcemia

70
Q

hypocalcemia s/s

A

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

71
Q

trousseau’s sign

A

BP cuff inflation = twitchy twitchyassoc with hypoca

72
Q

chvostek’s sign

A

poke cheeky = twitchy twitchyassoc with hypoca

73
Q

hyperca tx

A

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

74
Q

this lyte imbalance needs adjustment for hypoalbuminemia

A

hypocalcemia

75
Q

hypocalcemia tx

A

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!

76
Q

Ca replacement requiring central line

A

CALCIUM CHLORIDE

77
Q

PTH actions: effect, bone, gut, kidney

A

effect: ↑ Ca ↓ PO4bone: ↑ osteoclastsgut: indirect via vit Dkidney: Ca in PO4 out

78
Q

Vit D3: effect, bone, gut, kidney

A

effect: ↑ Ca ↑PO4bone: nonegut: ↑ Ca ↑PO4kidney: none

79
Q

serum bicarb + kidneys relationship

A

HCO3 takes time to change! high level = chronic acidosis causing bicarb to be retained in response

80
Q

BMP CO2 tells us what

A

it’s equivalent to HCO3 ABG BUT it is CO2 in serum NOT in gas (that’s ABG)

81
Q

THIS LYTE TAKES TIME TO CHANGE!!!!

A

HCO3 via kidneys

82
Q

elevated bicarb causes

A

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 #

83
Q

contraction alkalosis and volume relationship

A

volume CONTRACTION (depletion) hence the name!

84
Q

elevated bicarb tx

A

FIND CAUSEadjust pharmmaximize renal perfusion (consider supplementation if kidneys screwy)

85
Q

low bicarb causes

A

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

86
Q

** MUDPILES

A

gap acidosis (16+)M ethanolU remiaD KAP ropylene glycol I soniazidL actic acidosisE thylene glycol S alicylates

87
Q

elevated BUN causes

A

aka azotemiaAKICKDpre‐renal state (CHF, shock, hypovolemia)hypercatabolic state/steroidsupper GI bleedhigh protein feedingaggressive diuretic tx

88
Q

elevated BUN aka

A

azotemia

89
Q

low BUN… wtf?!

A

causes…younger agemalnourishedhemodilutionhepatic failure tx: given cause, is intervention really necessary?

90
Q

elevated BUN s/s

A

NEUROMUSCULAR- AMS- coma- encephalopathy- fatigue/weakness- myalgias- neuropathy- seizuresGIanorexia, nauseaGUamenorrhea, sexual dysfxnMISCaltered taste/smellsleep disturbancesuremic frost (N excreted via skin)

91
Q

uremic frost

A

N excreted via skin r/t elevated BUN

92
Q

elevated BUN tx

A

ID THE DAMN CAUSE- pathologic?- GI bleed, over diuresis, hyperalimentation?- pharmacologic?

93
Q

what is creatinine

A

catabolic byproduct of creatine phosphatereleased from muscle @ constant ratefiltered through kidneys (waste product) @ constant rateGFR marker

94
Q

what does a rise in creatinine indicate?

A

kidneys are excreting out less - GFR MARKER!DOES NOT MEAN MORE MADE

95
Q

elevated creat causes

A

impaired renal fxn: AKI, CKD

96
Q

low creat causes

A

muscle wasting ∴ mass loss- liver disease- malnutritionpregnancy

97
Q

elevated creat s/s

A

low‐grade feverfatigue/lethargy/malaiseanorexia, weight changedehydrationheadachedyspneamental status changes (encephalopathy)

98
Q

elevated creat tx

A

↓ production not possibleDETERMINE CAUSEdialysis: look at patient’s clinical picture to decide when

99
Q

how to tell if renal fxnal level appropriate?

A
  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
100
Q

phosphate #s

A

3 to 4.5 mg/dL

101
Q

dietary phosphate

A

red meat, fish, poultry, eggs, milk, whole grains, nuts, legumes ; cola beverages ; prepackaged fast foods; preservatives

102
Q

hyperphosphatemia is

A

greater than 4.5 mg/dLTYPICALLY WELL TOLERATEDeffects d/t hypocalcemia

103
Q

hyperphosphatemia s/s

A

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
Q

hyperphosphatemia tx

A

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
Q

hypophosphatemia causes

A
  • malnutrition/starvation- Mg & Al-based antacids- excessive phosphate binder - hyperparathyroidism- hyperalimentation (PO/PT/IV)- renal failure- EtOH abuse (lytes depleted)
106
Q

hypophosphatemia s/s

A

hypercalcemia!

107
Q

phosphate and calcium

A

BALANCE ∴ INVERSE RELATIONSHIP!hypocalcemia = hyperphosphatemiahypercalcemia = hypophosphatemia

108
Q

hypophosphatemia tx

A

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

109
Q

** hypophosphatemia: caution with IV repletion **

A
  • do not exceed 7 mmol/hr- K+ /Na+ supplementation
110
Q

best fluid for volume restoration

A

NORMAL SALINE!

monster management (29 decks)

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