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Clin med A 2 > Trigger - Fluid, Electrolyte, and Acid-Base Disorders > Flashcards

Trigger - Fluid, Electrolyte, and Acid-Base Disorders Flashcards

1
Q

Increased RAAS activity and SNS output is the body’s reaction to what

A

drop in osmotic pressure
also:
increased SNS output
increased RAAS activity
increased ADH levels
Increased thirst
decreased atrial natriuretic peptide (ANP)

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2
Q

decreased ADH levels and increased atrial natriuretic peptide is the body’s reaction to what

A

increase in osmotic pressure
also:
decreased SNS output
decreased RAAS activity
decreased ADH levels
decreased thirst
increased atrial natriuretic peptide (ANP)

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3
Q

etiologies include decreased PO intake, excessive fluid loss and third spacing

A

isotonic fluid volume deficit

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4
Q

s/s include AMS, weak pulse, hypotension, capillary refill of 2 seconds, and fatigue.

A

isotonic fluid volume deficit

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5
Q

Labs show:
high Uosm and Urine SG
increased Hct

A

isotonic fluid volume deficit

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6
Q

managed with admission of normal saline.

may also need Packed red blood cells or Inotropes

A

isotonic fluid volume deficit

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7
Q

when are inotropes indicated

A

poor cardiac output seen in isotonic fluid deficit

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8
Q

what is the cause of hyperchloremic metabolic acidosis. How do you treat this?

A

excess NS given for treatment of volume depletion

treat with bicarb solution (dextrose in H2O with HCO3)

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9
Q

when is mean arterial pressure used in the management of a patient

A

to assess the endpoint of treatment in patients being treated for isotonic fluid volume deficit

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10
Q

etiology includes over intake of salt such as during a state fair.

A

isotonic fluid volume excess

other etiologies include HF, renal failure and corticosteroids

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11
Q

etiologies include heart failure, renal failure, and corticosteroids

A

isotonic fluid volume excess

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12
Q

s/s are bloating, extremity edema, bulging neck veins, possible hypertension with full/bounding pulse.

A

isotonic fluid volume excess

general - decreased thirst, feeling bloated/swollen
CV - full, bounding pulse; distended neck veins, may see increased BP
High ECF - ascites, pulmonary edema, extremity edema

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13
Q

Labs:
abnormal renal labs
Low Uosm and Urine Sg
low Hct

A

isotonic fluid volume excess

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14
Q

labs:
abnormal renal labs
High Uosm and Urine sg
Low hct

A

isotonic fluid volume excess d/t inability to get rid of urine

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15
Q

Labs:
abnormal renal labs
Low Uosm and Urine sg
High Hct

A

Isotonic fluid volume deficit d/t renal fluid wasting

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16
Q

treatment plan includes:
restriction of fluid and sodium intake
furosemide (loops)
dialysis (if furosemide doesn’t work)

A

isotonic fluid volume excess

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17
Q

etiology includes impaired renal excretion of phospate

A

hyperphosphatemia

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18
Q

s/s include fatigue, SOB, N/V and +chvostek and trousseau’s

A

hyperphosphatemia

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19
Q

tx includes phosphate binders with meals and restoration of renal function

A

hyperphosphatemia, also obv limit intake of phosphate via processed foods

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20
Q

etiologies include:
use of diuretics, insulin, beta-agonists, or loops
OR
if patient is in alkalosis!

A

hypokalemia
also could be d/t intrinsic potassium wasting, metabolic acidosis, or hypomagnesemia

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21
Q

s/s include constipation, hypotension, palpitations, fatigue, cramps, dysrhythmias

A

hypokalemia

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22
Q

ECG shows flattened T waves -> prolonged QT -> U wave -> ST depression

A

hypokalemia

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23
Q

what is the management of acute severe hypokalemia

A

potassium replacement:
* oral or IV K chloride or K gluconate
* IV - 10-20mEq/hr max
* oral - 10-40 QD - QID

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24
Q

contributing factors include: hypomagnesemia and metabolic acidosis

A

hypokalemia

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25
Q

etiologies include: metabolic acidosis, adrenal insufficiency, hemolysis, cell damage and excessive/severe muscle contraction

A

hyperkalemia

causes include:
* Renal - inadequate excretion, metabolic acidosis
* Adrenal insufficiency
* Cellular breakdown - traumatic stick, hemolysis, crush injury
* Release from ICF - cell damage, excessive/severe muscle contraction
* Other causes - ACEI/ARB, beta-blockers, excess intake (usually IV)

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26
Q

etiologies include: traumatic stick, crush injury, or the use of ACEI/ARBs or BB

A

hyperkalemia

causes include:
* Renal - inadequate excretion, metabolic acidosis
* Adrenal insufficiency
* Cellular breakdown - traumatic stick, hemolysis, crush injury
* Release from ICF - cell damage, excessive/severe muscle contraction
* Other causes - ACEI/ARB, beta-blockers, excess intake (usually IV)

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27
Q

s/s include diarrhea, hypotension, palpitations, weakness, cramps, dysrhythmias, cardiac arrest

A

hyperkalemia

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28
Q

ECG - peaked T waves → loss of P waves → widened QRS → sine wave

A

hyperkalemia

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29
Q

what is the major difference in the s/s of hyperkalemia and hypokalemia

A

hyperkalemia presents with diarrhea, vomiting, cardiac arrest and no fatigue.

hypokalemia presents with fatigue, constipation and no cardiac arrest.

both present with cramps, hypotension, palpitations, dysrhythmias, and weakness. both present with ECG DIFFERENT ECG changes

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30
Q

what are the three steps to managing hyperkalemia

A

immediate clocking of cardiac effects
rapid reduction in plasma K+
removal of potassium

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31
Q

what is IV calcium gluconate used for?

A

reducing cardiac excitability in hyperkalemia.

IV calcium - reduced cardiac excitability
10mL of 10% calcium gluconate IV over 2-3 minutes w monitoring
repeat if ECG changes do not improve or recur in 1-3 minutes
may not be needed if there are no cardiac s/s or arrhythmias present

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32
Q

what interacts with IV calcium gluconate? How do we treat these pateitns?

A

digoxin!

patients taking digoxin are at risk for cardiac toxicity when given IV ca Gluconate.

give a SLOWER infusion of IV ca Gluconate to patients on digoxin.

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33
Q

when is insulin used in this lecture?

A

used alongside H2O and dextrose to reduce plasma volume of K+ in hyperkalemi.

can also add albuterol!

34
Q

What should be cautioned in CHF patients and is not an effective treatment in ESRD patients?

A

Albuterol and insulin + glucose in hyperkalemia to reduce plasma K+

35
Q

exchanges Na+ for K+ in GI tract which increases fecal excretion of K+

A

GI cation exchangers

36
Q

SE include hypernatremia, intestinal necrosis, constipation and fecal impaction

A

GI cation exchangers

37
Q

DDI with sorbitol and digitalis

A

GI cation exchanegrs

38
Q

DDI with Lithium, LT4 and metformin

A

GI exchangers

39
Q

DDI with antacids or laxatives with Al or Mg

A

Gi exchangers

40
Q

Avoid in post op patients or patients with a hx of renal transplant

A

GI cation exchangers

also wth hx of bowel obstruction, slow intestinal transit, or ischemic bowel disease

41
Q

A patient is hypervolemic with good renal function and hyperkalemia. what is the tx?

A

loop or thiazide diuretics

could use GI exchanger i think but i think the loops or thiazides are first line

42
Q

low Na with normal serum osmolality.

A

isotonic hyponatremia

43
Q

caused by extra molecules in the blood like protein and lipids

A

isotonic hyponatremia

44
Q

low Na with high serum osmolality

A

hypertonic hyponatremia

45
Q

caused by other molecules present in the blood such as glucose, radiocontrast, mannitol

A

hypertonic hyponatremia

46
Q

etiologies include burns, diuretics, intrinsic renal salt wasting

A

hypovolemic hyponatremia
also:
GI loss (N/V)
burns
dehydration
ACEi
diuretics
mineralocorticoid deficiency
intrinsic renal salt wasting

47
Q

etiologies include: N/V, dehydration, ACEI, mineralocorticoid deficiency

A

hypovolemic hyponatremia
GI loss (N/V)
burns
dehydration
ACEi
diuretics
mineralocorticoid deficiency
intrinsic renal salt wasting

48
Q

sodium is retained but water retention is disproportionately larger than Na retention

A

hypervolemic hyponatremia

49
Q

etiologies include:
nephrotic syndrome, liver disease, HF and intrinsic renal fluid retention

A

hypervolemic hyponatremia

50
Q

etiologies include hypothyroidism, psychogenic polydipsia, beer potomania, SIADH

A

euvolemic hyponatremia

51
Q

UNa+ and Uosm are used to assess what

A

ADH activity

52
Q

s/s include NV, HA, confusion and lethargy

A

early hyponatremia

53
Q

s/s include seizures, coma, brainstem herniation and death

A

late hyponatremia

54
Q

most s/s d/t cerebral edema

A

hypoatremia

55
Q

IV rehydration with isotonic .95 NS

A

tx for non severe hypovolemic hyponatremia.

also used to treat isotonic fluid deficit but with that you can also give PRBC and inotropes

56
Q

may co admin a loop to avoid volume overload and/or desmopressin to avoid osmotic demyelination syndrome

A

addition to treatment for severe hyponatremia

57
Q

what is treatment for severe hypovolemic hyponatremia

A
  • achieve 44-6mEq/L increase in sodium ASAP
  • repeat 1-2x at 10 min intervals if serum Na or s/s do not improve
  • monitor tx by measuring Na every 2 hours
  • may co admin a loop to avoid volume overload and/or desmopressin to avoid osmotic demyelination syndrome
58
Q

treatment includes hypertonic saline, salt tablets or fluid restriction

A

hypervolemic hyponatremia

59
Q

when do you use conivaptan or tolvaptan

A

nonemergent hyponatremia

(vasopressin receptor antagonists)

60
Q

CI for fluid restriction

A

vasopressin receptor antagonists

61
Q

Major SE hepatotoxicity. do not use for more than 30 days

A

vasopressin receptor antagonists

62
Q

monitor LFT, renal function and electrolytes with this treatment

A

vasopressin receptor antagonists (becasue hepatotoxicity)

63
Q

etiology is excessive water loss through renal or non renal sources

A

hypernatremia with normal Uosm

64
Q

etiology is neurogenic or nephrogenic DI

A

hypernatremia with low Uosm

65
Q

S/s include delirium, thirst, weak pulse, low BP, seizures

A

hypernatremia

Neuro - Increased thirst, HA, agitation, delirium, seizures, coma, death

CV - low BP, high HR, weak/thready pulse, dry mucous membranes, low skin turgor

66
Q

Labs:
Increased Hct

A

could be Hypernatremia
(would see abnormal Uosm, Urine SG, and renal labs)

could also be
isotonic fluid volume deficit

67
Q

tx: correction with fluid replacement within 24 hours to avoid CNS damage

A

hypernatremia present for less than 24 hours

68
Q

correction with fluid replacement gradually at 6-12 mEq/L per 24 hours

A

hypernatremia present for more than 48 hours

69
Q

etiologies include: hypokalemia, vomiting and gastric suction

A

metabolic alkalosis

also:
hypochloremia
hypokalemia
vomiting
Gastric suction
admin of bicarb/alkaline sol
diuretics
“perfect combo”

70
Q

etiologies include: hypochloremia and diuretics

A

metabolic alkalosis

also:
hypochloremia
hypokalemia
vomiting
Gastric suction
admin of bicarb/alkaline sol
diuretics
“perfect combo”

71
Q

etiology includes the combination of hypovolemia, hypochloremia, hypokalemia and reduced GFR

A

perfect setting for metabolic alkalosis

72
Q

s/s include dysrhthmias, dizziness, panic, lightheadedness, seizures.

A

metabolic alkalosis

may also see NV, abdominal pain and hx of GI suctioning

73
Q

etiology includes ketoacidosis and lactic acidosis

A

metabolic acidosis

also includes:
severe diarrhea
urine exposed to GI mucosa
distal or proximal tubular renal acidosis
ketoacidosis
lactic acidosis
decreased GFR

74
Q

etiology includes: severe diarrhea and urine exposed to GI mucosa

A

metabolic acidosis

75
Q

etiologies: decreased GFR

A

metabolic Acidosis

76
Q

s/s include vasodilation (flushing), constipation, confusion, weakness, drowsiness

A

metabolic acidosis

Neuro - decreased neuronal excitability - confusion, weakness, drowsiness
CV - vasodilation (flushing), dysrhythmias
GI - Abdominal pain, NVD, constipation
pulm - increased depth and rate of respiration
bone - decreased density with chronic

77
Q

decreased protein binding to calcium d/t decreased neuronal excitability

A

metabolic acidosis with hypercalcemia!

78
Q

s/s include muscle weakness, increased thirst and nephrolithiasis

A

metabolic acidosis with functional hypercalcemia

79
Q

tx includes decrease intake of animal content, especially proteins

A

chronic metabolic acidosis (main tx is HCO3 replacement

80
Q

etiology includes CKD, GI loss, renal tubular acidosis

A

CHRONIC metabolic acidosis

81
Q

how do you treat AKI with metabolic acidosis

A

dialysis and bicarb

Clin med A 2 (30 decks)

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