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CLIN MED II- NEPHRO/UROLOGY > FLUID BALANCE, HYPO/HYPERNATREMIA > Flashcards

FLUID BALANCE, HYPO/HYPERNATREMIA Flashcards

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1
Q

normal values
- plasma osmolality
- serum Na+

A

plasma osmo: 275-290
serum Na+: 135-145

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2
Q

inc vs dec plasma osmo

A

dec- during excretion, tonicity increases, ADH released and you retain water–> dec osmolality
- threshold is 280-290

inc- in dehydration, your plasma is more concentrated due to water loss
- threshold is 295

determinant of renal water excretion is ADH to osmoreceptors on basolateral membrane of prinicpal cells in collecting ducts

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3
Q

osmolarity v. tonicity

A

osmolarity- finding in a particular solution, what you measure in a test tube
- concentration of solutes in a solution

tonicity- effective osmolarity, in relation to membrane and permeability
- ex) isotonic, hypo, hyper

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4
Q

renal vs. extrarenal causes hypovolemia

A

RENAL
- diuretics
- osmotic diuresis
- hypoaldosterone state
- salt wasting (lose excessive salt in urine)
- diabetes insipidus

EXTRARENAL
- GI loss
- skin
- resp
- hemorrhage

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5
Q

hypovolemia associated clinical manifestations

A
  • related to dec CO
  • redistributional causes—> hypoalbuminemia, capillary leakage
  • sepsis
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6
Q

hypovolemia
- dx

A

full hx, physical
LABS:
BUN:creatinine ratio

  • normal 10:1 pre renal azotemia >20:1
  • urinary Na+ conc <20
  • urine osmo >450
  • specific gravity 1.015
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7
Q

hypovolemia tx

A

tx based on severity
- oral rehydration if mild
- IV fluid based on electrolyte abnorm and cause of hypovolemia

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8
Q

types of IV fluids
- distribution

A
  • normal saline: ECF replacement, distributed to interstitial
  • D5W: maintenance fluid, distributed through all fluid compartments
  • FFP: colloid, primarily intravascular
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9
Q

hyponatremia lab value

A
  • plasma Na+ <135
  • assoc with hypovolemia
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10
Q

hyponatremia
- SS
- dependent on?

A
  • asymp
  • nauseam, malaise
  • H/A, lethargy, confusion
  • stupor, seizure coma (severe)

severity dep on plasma level and rate of decrease

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11
Q

hyponatremia- labs

A

plasma osmo, urine osmo, urine Na+ conc, urine K+ conc

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12
Q

hyponatremia- plasma osmo
- high, normal, low causes

A
  • high: hyperglycemia, mannitol
  • normal: hyperproteinemia, HLD, s/p bladder irrigation
  • low: urine osmo <100 (primary polydipsia, reset osmostat), urine osmo >100 (eval ECF compartment volume status)
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13
Q

hyponatremia with LOW plasma osmo and NON-dilute urine (Uosm >100)
- ECF vol status (inc, norm, dec)

A
  • inc: CHF, cirrhosis, nephrotic syndrome, renal insuff
  • norm: SIADH, hypothyroidism, adrenal insuff
  • dec: urine Na <10 (extrarenal loss, remote vomiting, remote diuretic use) OR urine Na >10 (sodium wasting nephropathy, hyoaldosteronism, diuretic use, vomiting)
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14
Q

hyponatremia tx types

A
  • fluid restrictioon
  • salt restriction
  • loop diuretic
  • potassium replacement
  • NS via IV (nl saline)
  • hormone placement
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15
Q

hyponatremia rate of correction tx
- asymp vs emergency pts

A

asymp pt
- 0.5-1 mmol/L per hour
- do NOT correct >10-12 for first 24 hrs

emergency ss (coma, seizure)
- hypertonic saline, inc 1-2 for 3-4 hrs or until symp improve
- then follow asymp correction rate
- DO NOT correct >10-12 for first 24hrs

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16
Q

hypernatremia values

A
  • plasma Na+ conc >145 mmol/L
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17
Q

hypernatremia- renal loss of water
- drug induced v. osmotic

A

drug induced
- loop diuretics: isoosmotic diuresis, impaired concentrating ability of nephrons

osmotic
- mannitol, urea, glucose: impaired water reabsorp due to organic solutes in tubular lumen, water loss surpasses conc. ability
- these solutes draw water out

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18
Q

hypernatremia
- SS
- severity due to?

A
  • thirst/polyuria (mild)
  • alt mental status
  • weakness
  • neuro defects
  • seizure, coma (severe)

severity due to rate of change and severity of hypernatremia

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19
Q

expected body response to hypernatremia

A

max conc urine w minimal volume is 500 ml/day, urine osmo >800

thirst mechanism maintains adequate intake of free water to replace lost water

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20
Q

hypernatremia tx

A

tx underlying and correct water deficit

  • correct water deficit over 48-72 hrs
  • plasma Na dec limit to 0.5 per hr or 12 mmol/L per 24 hrs

same rule applies for hyponatremia

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21
Q

diabetes insipidus
- 2 types

A

nephrogenic v. central DI

  • nephrogenic: resistance to ADH/AVP secretion (kidneys fail to respond to ADH)
  • central: impairment of secretion (insuff production or release of ADH)
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22
Q

nephrogenic diabetes insipidus
- inherited v. acquired causes

A

resistance to ADH secretion

  • inherited: x linked rec v2 receptor gene, autosomal aquaporin 2 gene mutation
  • acquired: medications (lithium), hypercalcemia, hypokalemia, pregnancy (2nd-3rd trimseter)
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23
Q

central diabetes insipidus
- causes

A

impairment of ADH secretion
- mc cause: destruction of pituitary
- idiopathic or hereditary
- primary polydipsia (assoc w psych d/o or iatrogenic)

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24
Q

central vs. nephogenic DI tx

A

central
- intranasal desmopressin (synthetic ADH)
- low salt diet, low dose thiazide
- attempt meds that stim ADH secretion

nephrogenic
- tx underlying
- low salt diet, low dose thiazide
- NSAIDs
-** amiloride (K+ sparing) for pts taking lithium**

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25
dx central v. nephrogenic
fluid restrict pt, administer desmopressin - if Uosm inc by 50%--> central - Uosm unchanged---> nephrogenic (bc kidney function impaired)
26
hyperkalemia/hypokalemia labs specimens
sources: venous blood, arterial, urine - avoid drawing from limb with IV (stop IV for 30 mins and draw distal to IV site if needed) - dec hemolysis risk--> use large bore 18-20 gauge needle
27
how much absorbed and lost -potassium - when is there increased loss?
absorb 90% of consumed K+, GI loss 10% - inc loss in RENAL FAILURE, diarrhea w/large volume
28
renal excretion of potassium - dependent on?
- passive reabsorption in PCT and henle loop - active secretion in DCT and collecting duct by prinicpal cells - sec/reabsorp inc or dec based on K+ conc and aldosterone
29
Na/K/ATPase pump - potassium inc and dec based on?
sets up membrane potential, key to neuromusc function - INC pump activity by higher intracellular Na - DEC activity by digoxin tox, CHF, CRF - pump inhibited--> inc intracellular Na, inc K+ levels extracellular
30
potassium balance- renal - aldosterone - hyperkalemia - distal urinary flow - hypokalemia
- aldosterone: inc secretion - hyperkalemia: inc secretion - distal urinary flow: enhance excretion - hypokalemia: reabsorption inc
31
hyperkalemia- etiology/causes of potassium SHIFT
- rhabdomyolysis, hemolysis, burns, **strenous exercise**, sepsis - hypertonicity (K follows the flow) - insulin deficiency - Metabolic acidosis - pharmaceuticals (digoxin, B agonists, succinylcholine, arginine) ## Footnote all etiology that causes shift of K+ from inside the cell to outside!
32
hyperkalemia - etiology/causes of DEC EXCRETION
- renal failure, intertstitial nephritis, sickle cell ds - hypoaldosteronism (type IV RTA, diabetic nephropathy, heparin, end stage AIDS, adrenal insuff) - pharmaceuticals (ACEi, trimethoprim, NSAIDs, spirinolactone, triamterene, pentamadine) ## Footnote all etiology that results from dec renal function/excretion!
33
hyperkalemia- etiology of EXCESSIVE INTAKE
ingestion, iatrogenic
34
hyperkalemia - SS - PE
SS: none, weakness, palpitations, constipation PE: nl exam, irregular pulse rhythm, dec/absent bowel sounds, muscle weakness
35
hyperkalemia - lab result definitive - assoc tests - EKG changes
- K+ >5 - associated tests: BUN/creatinine, serum glucose, EKG, urine K+ and creatinine - EKG: peaked T waves, shortened QT
36
hyperkalemia - FEK renal vs extrarenal cause values
fractional excretion of potassium <10% = renal cause >10% = extrarenal cause
37
hyperkalemia - transtubular potassium gradient - extrarenal v renal cause values
gradient <6-8 = renal cause >8 = extrarenal cause >caveat: chronic renal failure CAN have >8
38
hyperkalemia - acute tx
OPTIONS - glucose and insulin - albuterol nebulized - calcium gluconate - diuretics - kayexalate - hemodialysis (LAST RESORT or if pt recovering do not want to overwhelm kidneys with meds)
39
hyperkalemia - chronic tx
- dietary restriction - removal of iatrogenic causes - loop diuretics - tx of route cause (fludrocotisone in hyporeninemic hypoaldosteronism)
40
hypokalemia - etiology
- renal potassium loss - potassium shift favoring intracellular - dec potassium intake (coupled w another cause) - extrarenal potassium loss - sample error
41
hypokalemia - etiology of renal potassium loss
- inc aldosterone effect (hypoaldosteronism, renovascular HTN, cushings, licorice, congenital anomaly/ 11beta or 17alpha hydroxylase def.) - inc flow at distal nephron (diuretics like furosemide or thiazides) - hypomagnesemia - renal tubular acidosis (fanconi syndrome, interstitial nephritis, metabolic alk) - genetic d/o (bartter's, liddle's) ## Footnote magnesium, calcium, and potassium usually follow each other!!!!
42
hypokalemia- etiology of potassium shift INTO cells
- insulin excess (post prandial, iatrogenic cause) - alkalosis (resp or metabolic) - B adrenergic excesses - hypokalemic periodic paralysis
43
hypokalemia- etiology of extrarenal losses
- vomit/diarrhea - villous adenoma (in GI tract) - zollinger-ellison syndrome (inc stomach acid)
44
hypokalemia - SS - PE
SS: none, muscle cramps, fatigue, weakness, constipation PE: - BP--> inc w aldosteronism, dec w/gitelmans and diuretic abuse - irreg HR - paralysis - decreased blood sugar
45
hypokalemia - dx
- dx lab result K+<3.5 - BUN/creatinine, glucose, magnesium, EKG, ABG, 24 hr urine potassium (for chronic)
46
hypokalemia - EKG
flat or inverted T waves, ST depression, prolonged PR
47
hypokalemia- urinalysis 24 hr urine vs transtubular potassium gradient - renal v extrarenal values
24 hr urine - <30 = extrarenal cause - >30 = renal cause transtubular potassium gradient - <2 = non renal cause - >3 = renal cause
48
# hypokalemia bartter's vs. gitelman's
bartters - hypokalemia - INC urine output - nl renal func - inc urine ions (Ca, K, Na, Mg, Cl) gitelmans - hypokalemia - NORMAL urine output - nl renal func - inc urine ions **- DEC URINE CALCIUM**
49
hypokalemia tx
- stable pt- tx underlying cause, eval diet for intake and meds that waste K - K+ replacement - role of magnesium replacement
50
hypokalemia tx - potassium replacement candidates - route of tx
pts that have: - hypokalemia - unable or unwilling to eat low sodium diet - n/v/d - unable to stop diuretic or laxative - drug related hypokalemia tx: - oral preferred - rate and site of IV important (suspend in saline, dont give faster than 40 mmol/hr, cardiac monitoring, K can be irritating to venous structures)
51
hypokalemia tx - magnesium replacement -
consider in cases of hypokalemia REFRACTORY to tx AND: - CHF, digoxin tox, chemo (cisplatin), loop diuretics
52
hypokalemia - follow up (emergency, stable, outpatient)
emergency: check electrolytes every 1-2 hrs or as conditions changes stable: 4-6 hrs after tx as condiiton change, then check daily outpatient: check weekly until stable, then monthly or quarterly dep on pt compliance
53
acid base disorders - nl pH - maintain pH by
nl pH: 7.35-7.45 maintain by cell/tissue buffering, pulm mechanisms (fast), renal mechanisms (slow)
54
acid base d/o - resp mechanism
regulate CO2, nervous sys reg resp rate - hypercapnia-- cause by hypoventilation - hypocapnia--- case by hyperventilation bicarb key
55
acid base d/o - renal mechanism
regulate plasma bicarb - reabsorp filtered bicarb - form titratable acid (normally phosphate related, ketoacids and creatinine can contribute) - excretion of NH4+ in urine
56
Acid addition (H+)
- ingestion proteins and fats - metabolic processes (aerobic/anaerobic, oxidative metab AA)
57
ABG procedure - errors?
- allen test, radial artery, syringe w 1cc fill, place on ICE send to lab, compress for 5 mins+, bandage - errors: air bubble in syringe, left too long for testing, venous draw
58
mixed acid base disturbance
when 2 or more primary d/o present in a pt - typical cause is diabetic ketoacidosis (metabolic) with asthma exacerbation (resp acid)
59
metabolic acidosis - HARDASS (non anion gap) - MUDPILES (high anion gap)
MUDPILES: methanol, uremia, diabetic keto, propylene glycol, INH, lactic acidosis, ethylene glycol, salicylates - also renal failure , EtOH HARDASS: hyperalimentation, addisons ds, renal tubular acidosis (type 1 and 2), diarrhea, acetazolamide, spirinolactone, saline - also ACEi, ARB, cyclosporine, trimethoprim, pentamidine, drugs (Ca, Mg)
60
drug induced acidosis
- salicylates : gastric lavage, Na Bicarb IV--> alk urine pH>7.5 - ethylene glycol (antifreeze) or methanol: thiamine and B6 suppl, saline diuresis, ethanol IV to compete w enzymes, dialysis
61
metabolic alk causes
- exogenous (bicarb IV or PO, milk-alkali syndrome) - gastric origin (vomit, aspirate, villous adenoma) - renal origin (diuretic, edema, post hypercapnia, recovery from acidosis, PCN, Mg/K def, bartter or gitelman) - high renin (RAS, HTN) - low renin (primary aldsoteronism, cushings, licorice) - liddles syndrome
62
resp acidosis vs alkalosis causes
acidosis: central, obstruct airway, parenchyma, neuromusc cause alkalosis: central, psychiatric, hypoxemia, drugs (salicylates), sepsis

CLIN MED II- NEPHRO/UROLOGY (16 decks)

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