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Medicine SHELF > Fluids, Electrolytes, Acid/Base > Flashcards

Fluids, Electrolytes, Acid/Base Flashcards

1
Q

What are the normal body fluid compartments?

A

TBW: 60%
ICF: 40%
ECF: 20%

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2
Q

What is the minimum amount of urine output needed to excrete products of catabolism?

A

500-600 mL/day

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3
Q

What does anasarca mean and when could it be found?

A

Whole body edema/extreme generalized edema; may be seen in patients with right sided CHF

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4
Q

When is NS used? What are the limitations?

A

Most common resuscitation fluid in hypovolemia
Limitations:
- Chloride load may lead to nonanion gap hyperchloremic metabolic acidosis if given in large boluses
- Only 25% of NS volume will remain intravascular

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5
Q

When is D51/2NS fluid used? What are the benefits?

A

Standard fluid maintenance

Contains some glucose which spares muscle breakdown, also has water for insensible losses

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6
Q

When is D5W used? What are the limitations?

A

Dilute powdered medications; provides free water to correct hypernatremia
Limitations:
- Only 8% remains intravascular because it diffuses into TBW; not effective in maintaining intravascular volume
- increases glucose in diabetic patients

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7
Q

When are LR used? What are the benefits and limitations?

A

Replacing intravascular volume only (not maintainance)
Benefits:
- no risk of hyperchloremic metabolic acidosis
Limitations:
- risk of hyperkalemia

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8
Q

What is colloid solutions? What are the limitations?

A

Albumin
Limitations:
- may cause harm in critically ill patients and TBI patients by shifting albumin into interstitial space
- not currently used

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9
Q 
What are the clinical symptoms of hypovolemia?
CNS
CV
Skin
GI
GU
A

CNS: AMS, sleepiness, apathy, coma
CV: orthostatic HPN, tachy, decreased PP, CVP, PCWP
Skin: poor skin turgor, hypothermia, cool/pale extremities, dry tongue and axilla
GI: ileus, weakeness
GU: decrease urine (compensatory, prenal azotemia)

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10
Q

What are the (4) classes of hypovolemic shock?

A

I <750: vitals signs normal, minimal sx
II <1500: tachycardia/pnea, normal BP, decreased urine
III <2000: “”, HPN at rest, very decreased urine (<22cc/hr)
IV 2000+: “”, little to no urine output

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11
Q

What are some laboratory values seen in hypovolemia and what do they indicate?

A
  • Na: increased in serum, decreased in urine
  • BUN:Cr >20:1
  • Hct: increase 3%/1L deficit OR decreased due hemorrhage
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12
Q

What fluids are used to resuscitate and/or maintain in hypovolemia?

A

Resuscitate: isotonic solution (LR, NS)
Maintenance: D51/2NS with 20mEq KCl/L

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13
Q

What are some causes of hypervolemia?

A

Iatrogenic (parenteral overhydration)

Fluid retaining states: CHF, nephrotic syndrome, cirrhosis, ESRD

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14
Q

What are the clinical symptoms of hypervolemia?

A

Weight gain
Vitals:
- HPN, hemodynamic instability if decompensated HF
- tachypnea, hypoxia if pulmonary edema present
PE
- peripheral edema: pitting, pedal, or sacral
- ascites: flank bulging and dullness, fluid wave, shifting dullness
- pulmonary edema: rales/dullness at lung base
- JVD
Labs
- low Hct, albumin
- hypoNa
Swan-Ganz cathter
- elevated CVP, PCWP

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15
Q

What is the most sensitive sign of hypervolemia? What is the most specific sign?

A

Sensitive: flank bulging and dullness
Specific: fluid wave

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16
Q

What is the treatment plan for hypervolemia?

A
  • Fluid restriction
  • Diuretic use
  • Monitor daily UO, weights, consider Swan-Ganz catheter placement
  • urgent dialysis if hemodynamically unstable and initial attempts are unsuccessful
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17
Q

What is the difference between [Na] and Na content?

A

[Na] indicates water homeostasis

Na content indicated sodium homeostasis

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18
Q

Where is the sodium cation primarily located? Intracellular or extracellular?

A

Extracellular, active pumped out of cells

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19
Q 
What happens to the levels of the following hormones when there is an increased in sodium intake? Why?
ECF volume
GFR
Sodium excretion
Renin
Norepinephrine
Epinephrine
Aldosterone
ADH
A
  • ECF volumes increases
  • leads to increase in GFR and sodium excretion through ANP/BNP from the heart + decreased renal renin release
  • causes natriuresis
  • inhibits NE, EP, ALD, ADH
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20
Q

What does aldosterone do to the levels of sodium and potassium in the late distal tubules? What happens to water?

A
  • Increase sodium reabsorption; water follows sodium

- Increase potassium secretion

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21
Q

Where does the majority of sodium reabsorption occur? How do the following medications work to inhibit sodium reabsorption?
Furosemide / loop diuretics
Thiazide diuretics

A

Most sodium reabsorption occurs in proximal tubules

  • loop diuretics: inhibit Na-K-Cl transporter in thick ascending loop of Henle
  • thiazide: inhibit Na-Cl transporter in early distal tubule
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22
Q

Activation of what stimulators produces thirst?

A

Osmoreceptors in the hypothalamus stimulated by hypertonicity

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23
Q

How does ADH work and from where is it released?

A

Posterior pituitary gland releases ADH when plasma tonicity increases, ADH binds to V2 receptors in renal collecting ducts

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24
Q

Below what level do symptoms of hyponatremia begin? What is the exception?

A

Symptoms at <120
- in ICP, correction of hyponatremia with fluids causes water to shift into brain cells, worsening ICP; important to keep sodium levels normal or slightly high in ICP

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25
What laboratory value is used to differentiate evaluate kidney function in hypovolemic hypotonic hyponatremia? What does it indicate?
Urine sodium - Low: increased sodium retention by kidneys to compensate for extrarenal losses - High: tubular dysfunction due to inability of tubules to reabsorb sodium (ACEi, ATN, diuretic excess, decreased aldosterone)
26
What are (6) causes of euvolemic hypotonic hyponatremia?
1. SIADH 2. Hypothyroidism 3. Adrenal insufficiency 4. Psychogenic polydipsia 5. Excess free water (administration or intake) 6. Low dietary intake
27
What are some common causes of SIADH?
- CNS pathologies - Malignancy: small cell lung cancer - Surgical - postop - Medications: SSRI, oxytocin, carbamazepine, haloperidol, cyclophosphamide, antineoplastic agents - Infections: HIV, pulmonary infxns
28
What are (3) common causes of hypervolemic hypotonic hyponatremia?
1. CHF 2. Nephrotic syndrome 3. Liver disease
29
What is pseudohyponatremia and what are it's causes?
Isotonic hyponatremia - Normal amount of serum sodium, but increase in plasma solids (lipids, proteins) causes an artificial laboratory decrease in [sodium]
30
What causes hypertonic hyponatremia? What are some examples? What are their treatments?
Osmotic substances cause osmotic shift of water out of cells causing osmotic gradients - glucose: every +100mg/dL glucose = (-)3 mEq/L Na - mannitol, sorbitol, glycerol, maltose - radiocontrast agents Treatment: treat underlying cause
31
What organ system is affected most by hyponatremia? What are the symptoms?
Neurological system due to cerebral edema - HA, delirium, irritability - muscle twitching, weakness - hyperactive DTR
32
``` What are symptoms of hyponatremia by organ system? Neurological CV GI GU ```
``` Neurological: HA, delirium, irritable, increased DTR, salivation, lacrimation CV: HTN due to ICP GI: n/v, ileus, watery diarrhea GU: oliguria -> anuria MSK: muscle twitching ```
33
How is hypoNa diagnosed? How is it treated?
Diagnosis: - Plasma osmolality: low in true hyponatremia - Urine osmolality: low if kidneys functioning; high if ADH - Urine [sodium]: should be low in true hypoNa, <25 in hypovolemia, 20-40 if SIADH/salt-wasting, hyperALD Treatment:
34
What is the treatment in hypovolemic hypotonic hypoNa for the following Na levels? Mild: 120-130 Moderate: 110-120 Severe: <110
120-130: hold free water, observe, (+) salt tablets in SIADH 110-120: loop diuretics + saline <110: hypertonic saline (+)1-2 mEq/L/hr until sx resolve **do not (+)>8mEq during first 24h due to risk of central pontine demyelination
35
What are some causes of hypovolemic hyperNa (more water is lost compared to Na loss)? How is it treated?
Renal loss: diuretics, osmotic diuresis (glucosuria), renal failure Extrarenal loss: diarrhea, diaphoresis, respiratory losses Treatment: (+) isotonic NaCl to restore euvolemia first, then replace free water defecit
36
What are the causes of euvolemic hyperNa (Na stable, water lost)? How is it treated?
- Diabetes insipidus (central): CNS pathologies - Diabetes insipidus (peripheral): lithium toxicity, hyperCa, hypoK, renal disease, drugs - Insensible respiratory losses Treatment: vasopressin, low Na diet, thiazide diuretics, oral fluids or D5W
37
What are the causes of hypervolemic hyperNa (excess Na - rare)? How is it treated?
- Iatrogenic (mc): large parenteral NaHCO3, TPN - Exogenous glucocorticoids - Cushing's syndrome - Saltwater drowning - Primary hyperALD Treatment: Diuretics (furosemide) for volume correction, D5W to establish normal [Na]; balance to remove excess sodium. Dialyze in patients with renal failure
38
What are the clinical symptoms of hyperNa?
Neurological: AMS, restlessness, weakness, focal defects, confusion, seizures, coma General: tissue and mucous membranes dry; decreased salivation
39
How is hyperNa diagnosed?
Low urine volume | High urine osmolality >800
40
What is used to differentiate between nephrogenic and central diabetes insipidus?
Desmopression
41
What are the two different rules used in calculation of maintenance fluids?
100/50/20 rule: (first 10 kg*100, second 10 kg*50, 20/kg >20)/24 4/2/1 rule: 4*10kg + 2*10kg + 1*n/kg
42
What are the (3) main things that affect Ca levels? In what ways?
1. Hormones - PTH - affects free, active Ca ions 2. Albumin - most calcium ions are bound to albumin, therefore [albumin] affects total [Ca] 3. pH - changes Ca bound to albumin; higher pH means more Ca bound to albumin (alkalotic states may cause decrease in free Ca leading to sx of hypoCa)
43
What are the (3) hormones that affect calcium levels? How do they affect the levels of phosphorus?
1. PTH: increased plasma Ca, decrease plasma PO4 2. Calcitonin: decrease plasma Ca, decrease plasma PO4 3. Vitamin D: increase plasma Ca, increase plasma PO4
44
What organ systems are acted upon in calcium and phosphorus homeostasis?
Bone Kidneys Gut
45
What are (12) causes of hypoCa?
1. HypoPTH - usually due to collateral damage during thyroid surgery 2. Renal insufficiency - due to decreased 1,25 VitD 3. Vitamin D deficiency 4. HyperPO4 - bonds with Ca to form CaPO4 deposits 5. HypoMg - causes decreased PTH; from malabsorption 6. PseudohyperPTH - AR dz causing organ resistance to PTH 7. HypoALB - total Ca decreased, but clinically fine since free Ca is still normal 8. Alkalemia - increased Ca binding to albumin, therefore decreased free, active Ca 9. Acute pancreatitis - Ca deposits decrease serum Ca 10. Blood transfusion w/citrated blood - citrate binds Ca 11. Osteoblastic metastasis 12. DiGeorge syndrome
46
What are the organ systems affected by hypoCa? What are the symptoms?
Neurological: numbness/tingling in fingers and toes, tetany, increased DTR, chovstek sign, trousseau sign, seizures // BG calcifications CV: arrthymias, prolonged QT MSK: rickets, osteomalacia
47
What happens to the levels of PO4 in the following conditions? Renal insiffuciency HypoPTH Primary Vitamin D deficiency
Renal insufficiency: high HypoPTH: high Primary Vitamin D deficiency: low
48
``` What happens to the levels of PTH in the following conditions? HypoPTH Vitamin D deficiency CKD PseudohypoPTH ```
HypoPTH: low Vitamin D deficiency: high CKD: high PseudohypoPTH: extremely high
49
``` What are the treatments for hypoCa? Symptomatic Long-term management PTH deficiency What additional electrlyte must also be corrected? ```
Symptomatic: IV calcium gluconate Long-term management: PO Ca + vitamin D PTH deficiency: PO Ca + vitamin D, thiazide diuretics to prevent Ca stones from forming **correct Mg in addition to/before Ca correction
50
What are the (4) main causes of hyperCa?
1. Endocrinopathies 2. Malignancies 3. Pharmacologic 4. Other
51
What endocrinopathies may cause hyperCa? Why?
HyperPTH - adenoma leads to increased Ca, low PO4 Renal failure - if secondary hyperPTH desensitizes the parathyroid to calcium levels, PTH may rise enough to cause hyperCa (tertiary hyperPTH) Paget disease of the bone - osteoclastic bone resorption Addison disease
52
What malignancies may lead to hyperCa? Why?
Metastatic cancer - bony mets leads to osteoclastic lesions Multiple myeloma - lysis of bone by tumor cells, myeloma cells release osteoclast-activating factor Squamous CC of lung, head/neck - PTHlike hormone Lung, ovarian cancer - PTH release Lymphomas - vitamin D release
53
What pharmacologic causes may lead to hyperCa? Why?
1. Vitamin D intoxication - high GI reabsorption 2. Milk-alkali syndrome - excessive intake (antacids, milk) causes alkalosis and renal impairment 3. Thiazide diuretics - inhibit renal excretion 4. Lithium - PTH levels increase
54
How do the following diseases cause hyperCa? Sarcoidosis Familial hypocalciuric hypercalcemia
Sarcoidosis - increased GI absorption | Familial hypocalciuric hypercalcemia
55
What are the symptoms of hyperCa? (Hint: there is a mnemonic)
Stones (due to hypercalciuria) Bones: bones aches and pains Groans: muscle pain, weakness, pancreatitis, peptic ulcer disease, gout, constipation Psychiatric overtones: depression, fatigue, anorexia, sleep disturbances, anxiety, lethargy Other: polydipsia, polyuria, nephrogenic DI, HTN, (-)w, shortened QT
56
What does an elevation in PTHrP indicate about the cause of hyperCa?
Likely due to malignancy
57
What are the treatment options used in hyperCa? (Most cases only require treatment of underlying disease)
1. Urinary excretion - IV fluids, diuretics 2. Inhibit bone resorption in patients with osteoclastic disease - bisphosphonates, calcitonin 3. Glucocorticoids only if related to vitamin D or multiple myeloma 4. Hemodialysis in renal failure patients
58
What is the risk of using phosphate replacement in patients with hyperCa?
Metastatic calcification
59
Where does the majority of potassium excretion occur? What hormone plays an important role in its excretion?
Excretion occurs mostly in the kidneys (80%) through the levels of aldosterone. The rest is excreted through the GI system
60
What are the main causes of hypoK in the following systems: GI Renal
GI: Vomiting, NG drainage, diarrhea, laxatives/enema, intestinal fistulas (IBD-Chron's, diverticulitis), decreased absorption in GI disorders Renal: diuretics, RTD, hyperALD, excess glucocorticoids, Mg deficiency, Bartter syndrome
61
How does excess glucocorticoids cause hypoK?
Glucocorticoids exert mineralocorticoid action at high serum levels
62
What is Bartter syndrome?
AR defect in salt reabsorption leading to increased renin levels, secondary ALD elevations, and chronic volume depletion
63
What are non-GI or renal causes of hypoK?
``` Low dietary intake Insulin Antibiotics - amphotericin B Profuse sweating Epinephrine (B2-agonists) ```

Medicine SHELF (13 decks)

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