Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Nephrology > Fluids- electrolytes > Flashcards

Fluids- electrolytes Flashcards

1
Q

Components of body fluid?

A
  • ICF: 2/3 of total body fluid
    -ECF: 1/3
    ISF, plasma, and lymphatic fluid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Electrolytes in ECF and ICF?

A
  • ECF: Na+ (142 mEq/L), Cl- (103 mEq/L), HCO3-

- ICF: K+ (140 mEq/L), Mg, phosphates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Water movement regulation?

A
  • starling forces: hydrostatic pressures and osmotic pressures:
    Capillary hydrostatic pressure: pressure in capillary pushing fluid out
    Interstial fluid hydrostatic pressure: pushing fluid in from ISF
  • Osmotic force due to plasma concentration (drawing fluid into capillaries)
  • Osmotic force due to ISF protein concentration (drawing fluid out)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is osmolality? What is most important factor?

A
  • concentration of an osmotic soln when measured in osmols of solvent
    plasma: 280-295 mOsm/kg
  • Na+ is most impt plasma osmolality factor (water follows Na+)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Process of fluid and electrolyte replacement? IV solutions?

A
  • assess ins and outs
  • oral replacement preferred when tx dehydration
  • IV:
    saline equivalents: crystalloids - normal saline or LR
    water equivalents: D5W
    if 3% NS - have to do central line (will destroy peripheral veins)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the components of LRs?

A
  • 250-273 mOsm/L

- Na+, Cl-, lactate, Ca+, K+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Parenteral colloids?

A

isotonic
- albumin: 290-31- mOsm/L
- blood products:
packed RBCs, fresh frozen plasma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Saline: 3%, 5%, D5W1/2NS adverse effects?

A
  • ICF depletion
  • fluid overload
  • hypernatremia
  • hyperchloremia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Albumin adverse effects?

A
  • allergic reactions

- possible infection transmission (hepatitis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Impt steps in assessing types of fluid loss?

A
  • pt hx
  • sxs
  • vital signs and PE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is hypervolemia?

A
  • too much Na+
  • expansion of effective arterial blood volume
  • CHF, cirrhosis, aldosterone, renal disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

WHat is hypovolemia?

A
  • too little Na+
  • volume contraction
  • dehydration: V/D, exercise, not drinking enough water
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is hyponatremia? Hypernatremia? Edema?

A

hyponatremia:

  • too much water
  • not enough Na+

hypernatremia:

  • too little water (dehydration)
  • excess Na+

edema: too much Na+ with water retention in the ISF (abdomen, lungs) - alcoholics, cirrhosis, metastatic cancers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Severity of edema?

A
  • 1+ = 2 mm
  • 2+ = 4 mm
  • 3+ = 6 mm
  • 4+ = 8 mm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How to tx mild dehydration?

A
  • oral replacement:
    fluids with electrolytes are preferred
  • avoid fluids with high sugar concentration
  • water and sports drink or in children pediolyte
  • stop activities that create ongoing losses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Assessing degree of fluid loss for moderate hypovolemia?

A
  • hx: any GI losses (V/D), excessive exercise, renal losses
  • sx: easy fatiguability, thirst, muscle cramps, postural dizziness, abdominal pain, CP, lethargy, confusion, decreased urination
  • clinical manifestations: decreased skin turgor, tachycardia, dry mucus membranes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How do electrolyte imbalances present? How do these imbalances occur?

A
  • sxs: precipitate as CV, neuro, and neuromuscular abnormalities
  • disruptions occur: via drugs, disease states, diarrhea, vomiting, infection, hormone imbalances, malignancies
  • to tx these: need results of lab tests then start IV fluids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Etiologies of hyponatremia?

A
  • hypovolemia: GI losses: vomiting, and diarrhea, dehydratioon
    renal losses: (thiazide diuretics), ACEIs, mineralocorticoid deficiency
  • normovolemia: SIADH, primary polydipsia/marathon runners, low dietary solute intake, psychogenic polydipsia
  • hypervolemia: CHF, cirrhosis, nephrotic syndrome, advanced syndrome (rare)
  • others: hypothyroidism, primary adrenal insufficiency, drugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What lab values do you want to know for hyponatremia? lab value indications?

A

hyponatremia is less than 135 meq/L
- serum osmolality impt
- urine Na+
- assess severity:
less or equal to 120 meq/L panic value***
- 120-130: depends on sxs and situations
- greater than 130 is generally not tx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Clinical manifestations of chronic hyponatremia?

A
  • cerebral adaption:

going to have fatigue, nausea, dizziness, confusion, lethargy, muscle cramps, gait disturbances and forgetfulness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Clinical manifestations of acute hyponatremia?

A
  • acute hyponatremic encephalopathy: cerebral over hydration related to degree of hyponatremia
    fatigue an malaise are usually the first sxs
  • HA, lethargy, coma, seizures and eventually respiratory arrest
  • acute hyponatremic encephalopathy may cause permanent neuro damage or death
  • can be hyponatremic classified by ECF status: hypovolemic: GI losses, renal losses (thiazides), normovolemic: SIADH, low Na+ intake, hypervolemic: CHF, cirrhosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How does osmotic demyelination happen?

A
  • try to correct hyponatremia and then you overcorrect making ECF hypernatremic so H2O leaves brain too quickly and it shrinks
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How can acute hypotonic hyponatremia occur? WHat are the sxs?

A
  • can result in sxs of neuronal cell expansion and cerebral edema
  • Nausea/HA, seizure, coma and death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Hyponatremia etiologies with inability to suppress ADH problem?

A
  • true volume depletion (GI or renal losses - thiazide diuretics), decreased tissue perfusion (reduced CO or systemic vasodilation in cirrhosis for instance)
    syndrome of inappropriate ADH secretion (SIADH)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Causes of hyponatremia with appropriate suppression of ADH secretion?

A
  • primary polydipsia
  • low dietary solute intake
  • advanced renal failure
26
Q

Causes of hypovolemic hyponatremia?

A
  • GI or renal losses
  • if serum Na+ hasn’t dropped critically low quickly
  • usually just volume replacement orally or IV if more severe
27
Q

Tx for hypovolemic hyponatremia?

A
  • NS/isotonic saline
  • depending on pt status may do slow bolus
  • then maintenance depending on ongoing losses
28
Q

Causes of hypervolemic hyponatremia?

A
  • CHF, cirrhosis, renal failure
29
Q

Tx of hypervolemic hyponatremia?

A
  • restrict fluids: 1000-1200 ml/day
  • restrict sodium: 1000-1200 mg/day
  • utilize loop diuretics to remove excess fluid, K+ replacement
30
Q

What is SIADH? Causes? Tx?

A
  • too much ADH. Either Eu/hypervolemic hypotonic hyponatremic presentation

can be:
drug induced: carbamazepine, SSRIs, haloperidol, and thorazine

disease induced: malignancies, CNS disorders, post-surgery, pulmonary infections

Tx: tx underlying cause, fluid restriction is mainstay!!!!! May use oral salt tablets, loop diuretics

31
Q

What is the therapy for severe hyponatremia?

A
  • this puts pt at risk for brain herniation
  • tx: 3% hypertonic saline:
    goal to increase Na+ by 4-6 meq/L in 24 hr period, measure serum Na+ q hr, and measure urine output
32
Q

What risk is there if you correct severe hyponatremia too rapidly? What are the high risk populations?

A
  • develop osmotic demyelination
    High risk pops:
  • women and children postop period
  • pts with hyperacute hyponatremia - psychosis, marathons, ectasy, and those with intracranial pathology
33
Q

hypernatremia: etiologies?

A

Unreplaced water loss:

  • impairment in thirst or access to water
  • insensible and sweat losses
  • GI losses
  • central or nephrogenic diabetes insipidus
  • hypothalamic lesions impairing thirst or osmoreceptor fxn:
  • primary hypodipsia
  • reset osmostat in mineralorticoid excess

water loss into cells:
severe exercise or seizures

sodium overload:
intake or administration of hypertonic sodium solns

34
Q

Acute hypernatremia manifestations?

A
  • rapid decrease in brain volume can rupture cerebral veins leading to focal intracerebral or subarachnoid hemorrhage
  • demyelinating brain lesions as seen with overly rapid correction of chronci hyponatremia
35
Q

Chronic manifestations of hypernatremia?

A
  • brain adapts (within a day) by pulling water from the CSF and increasing the uptake of solute by the cells which also increases the amt of water into the cells
  • assessment is difficult because most affected adults already have neuro disease diminishing the thirst response
36
Q

Etiology of hypernatremia (greater than 145 meq/L?

A
  • loss of water
  • addition of hypertonic soln
  • sodium overload
37
Q

Tx of hypernatremia?

A
  • replace free water with D5W, add normal saline soln if hypovolemic - use a seond IV
  • if replacing ongoing electrolyte losses (use 0.45% NS possibly with added K+)
  • fast onset, less than 24 hrs, decrease by 1 meq/L/hr correction
  • insidious is greater than 24 hrs, decrease in serum Na+ by no more than 10 mEq/24 hrs
  • monitor serum Na+/K+ closely
38
Q

What is central DI? what is the tx?

A
  • not enough ADH production (tumors, or lesions on the brain)
  • tx: desmopression: 10 mcg/day, ADH like activity
  • titrate to 10 mcg/bid intranasally, and restrict fluid intake
39
Q

What is nephrogenic DI? Tx?

A
  • kidney resistant to ADH

- tx: thiazide diuretic to decrease ECF and Na+, Na+ restriction (2000 mg/day)

40
Q

How do you tx hypernatremia?

A
  • for hypernatremia from unreplaced water loss:
    need to est water deficit
  • need to replace ongoing losses, any ongoing GI losses and urine losses
  • obligatory losses: sweat and stool
  • determin safe rate plasma Na+ can be normalized:
    usually less than 0.5 mEq/L/hr or about 10 mEq/day, usually use 0.45% NS with K+
  • monitor lytes closely (q 4 hrs)
  • overly rapid correction: can lead to cerebral edema
41
Q

What percentage of Ca2+ is bound to albumin? Where is calcium normally found?

A
  • 46%
  • each 1 g/dL drop of albumin below 4.5g/dL, decreases serum calcium by 0.8 mg/Dl
  • when you look at Ca2+ levels make sure you are looking at albumin levels too if Ca levels are off
  • it is an extracellular electrolyte, and it is in an unbound/free fraction active form
  • normal serum range (free): 8.5-10.5 mg/dL
42
Q

Etiologies of hypercalcemia?

A
  • greater than 10.5
  • cancer and primary hyperparathyroidism (primary causes
  • drugs: thiazide diuretics, calcium supplements, lithium
43
Q

Sxs of hypercalcemia? What can occur if left untx?

A

EKG changes
N/V, anorexia, constipation
polyuria/dypsia
neuro/psych sxs

  • if left untx:
    metastatic calcification, nephroliathisis, renal failure
44
Q

Outcome and tx of hypercalcemic crisis?

A
  • outcome: oliguric renal failure, coma, v-arrhythmias, death
  • tx: saline and loop diuretics: 2-3 mg/dL, drop in 24-48 hrs
    bisphophonates: for malignant etiologies: zoledronic acid: 4 mg IV over 15 min
  • osteoclast inhibitors: calcitonin
  • dialysis
45
Q

Etiologies of hypocalcemia? sxs?

A
  • hypoparathyroidism, vit D deficiency, loop diuretics, and high or normal phosphates
  • correct level for hypoalbuminemia
  • hypomagnesemia assoc with refractory severe hypocalcemia
  • sxs: tetany, paresthesias around mouth - hallmark sxs
  • EKG: QT prolongation, decreased myocardial contractility
46
Q

How do you tx acute sx HypoCa++?

A
  • IV admin of calcium salts
  • 100-300 mg elemental calcium IV over 5-10 min (less than 60 mg/min)
  • continuous infusion: 0.5-2 mg/kg/hr for 2-4 hrs
  • maintenance infusion 0.3-0.5 mg/kg/hr
  • gluconate over chloride for peripheral admin because of less irritation
  • Magnesium if hypomagnesaemia present
47
Q

How do you tx chronic hypocalcemia?

A
  • oral calcium supp (give Vit C with Ca, and Vit D if not responding)
  • 1-3 grams elemental calcium/day: watch for -
    constipation, GI upset, carbonate less expensive than gluconate/citrate , but citrate better absorption
  • if not responding - add vit D: 1000 IU/day
48
Q

Normal serum level of phosphorus? Hyperphosphatemia? Tx?

A
  • 2-4.5 mg/dL
  • hyperphosphatemia: decreased excretion due to low GFR (renal disease), chemo and rhabdomyolysis
  • sxs due to Ca-phosphate interaction
  • hypocalcemia results with chronic hyperphostphatemia
  • tx: GI binders - IV Ca++ salts
49
Q

Tx of hyperphosphatemia?

A
  • emergency tx seldom necessary: this can be done with dialysis
  • usually occurs in renal failure:
    diet restriction, phosphate binding gel: selvelamer (decreases mortality), calcium supplements, avoid aluminum containing antacids - this can cause bone disease
50
Q

What is hypophosphatemia? sxs? Tx?

A
  • less than 2.0
  • sxs are rare until under 1 mg/dL
  • long term: proximal muscle weakness and osteomalacia
  • severe or sx hypophosphatemia:
    IV phosphorus - give slowly, NaPO4, K+PO4
  • oral phosphate replacement for mild to moderate:
    neutra-phos
  • neutra-phos K: 250 mg phosphate, GI upset
51
Q

Causes of hypomagnasemia?

A
  • reduced intake: dieting, unbalanced diet, depleted foods
  • impaired absorption (malabsorption) - GI diseases -IBD - crohns, ulcerative colitis
  • increased excretion: alcoholism, laxative abuse, tx with diuretics or digitalis
52
Q

Clinical manifestations of hypomagnesemia? drugs that can cause this?

A
  • occurs in nearly 12% of hospitalized pts
  • manifestations: neuromuscular, muscle cramps, tetany, seizures, coma
    abnormalities of Ca metabolism - hypocalcemia, CV: widened QRS, a fib, ventricular arrhythmias
  • drugs that can cause this: diuretics, aminoglycosides, cisplatin, cyclosporine, and alcohol
53
Q

When and what should you tx hypomagensemia with?

A

hypomag: is less than 1.4 mEq/L
- tx if less than 1 mEq/mL or sx
- Tx with:
IV MgSO4 if sx/severe:
bolus - can cause flushing, sweating
- a large amt is secreted in the urine so a continuous infusion is need after the bolus to raise the magesium level
- oral replacement if mild-mod:
sustained release preps preferred
otherwise usual dosing 800-1600 mg a day in divided dosing, often causes diarrhea

54
Q

hypermagnesemia sxs?

A
  • Mg 3-5 meq/L: N/V
  • Mg 4-7 meq/L: sedation, decreased reflexes, weakness
  • Mg 5-10 meq/L: hypotension, bradycardia, quadriplegia
  • Mg 10-15 meq/L: no reflexes, respiratory paralysis, cardiac arrest
55
Q

Tx of hypermagensemia?

A
  • greater than 2 mEq/L
  • IV calcium (100-200 mg elemental Ca++) to antagonize neuromuscular and CV effects of magnesium
  • tx: renal failure: hemodialysis
    if normal renal function: forced diuresis with fluid and loop diuretics
56
Q

Hypokalemia? Etiologies? Sxs?

A
  • less than 3.5 mEq/L
  • etiologies: B-2 agonists, loop diuretics, ACEIs, thiazides, High dose PCNs, amphotericin B, insulin
    medical: metabolic acidosis, vomiting, diarrhea
  • sxs: low energy, muscle weakness, restlessness, cardiac sxs: EKG changes: U wave, cardiac arrhythmias
  • danger in persons on digoxin
57
Q

Hypokalemia tx?

A
  • loop or thiazide deficit:
    40-100 mEq K supp (BID or TID)
    oral therapy is preferred: KCL (given in mEq not mg)
  • without food to avoid GI upset
  • severe or sx:
    IV K in saline bag: dextrose stimulates insulin to further shift K into cells so don’t give dextrose!!!
  • 10-20 mEq KCL in 100 mL 0.9% saline over one hour
  • more than 10 meq/hr monitor EKG
  • limit 40-60 mEq/L peripheral line: phlebitis
58
Q

Etiologies of hyperkalemia?

A
  • greater than 5.5 mEq/L
  • increased K+ intake
  • decreasd excretion
  • aldosterone resistance
  • shift to ECF (in DKA)
59
Q

Clinical manifestations of hyperkalemia?

A
  • ascending muscle weakness
  • usually doesn’t affect respiratory muscles
  • cardiac effects: EKG changes: initially peaked T waves and shortened QT interval, which progresses to prolonged QRS and QT interval and P waves may disappear, can can then lead to dysrhythmias
60
Q

Tx of hyperkalemia?

A
  • abnorm EKG: calcium gluconate IV (just tx cardiac effects)
  • give D5W to create hyperglycemic state then insulin (make sure doesn’t become to hyperglycemic)
  • consider bicarb if acidotic: H+ exchanged for K+ in ICF to compensate for acidosis: bicarb reverses this
  • renal failure: dialysis, K binders: Na polysterene sulfonate (kayexelate) exchanges Na for K in gut: constipation
  • loop diuretics if not volume depleted or kidney disease

Nephrology (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions