Brainscape's Knowledge GenomeTM

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


See full index

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%

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

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

A

500-600 mL/day

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

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

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

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

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

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

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

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are some causes of hypervolemia?

A

Iatrogenic (parenteral overhydration)

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

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

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

A

[Na] indicates water homeostasis

Na content indicated sodium homeostasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

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

A

Extracellular, active pumped out of cells

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Activation of what stimulators produces thirst?

A

Osmoreceptors in the hypothalamus stimulated by hypertonicity

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What laboratory value is used to differentiate evaluate kidney function in hypovolemic hypotonic hyponatremia? What does it indicate?

A

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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are (6) causes of euvolemic hypotonic hyponatremia?

A
  1. SIADH
  2. Hypothyroidism
  3. Adrenal insufficiency
  4. Psychogenic polydipsia
  5. Excess free water (administration or intake)
  6. Low dietary intake
27
Q

What are some common causes of SIADH?

A
  • CNS pathologies
  • Malignancy: small cell lung cancer
  • Surgical - postop
  • Medications: SSRI, oxytocin, carbamazepine, haloperidol, cyclophosphamide, antineoplastic agents
  • Infections: HIV, pulmonary infxns
28
Q

What are (3) common causes of hypervolemic hypotonic hyponatremia?

A
  1. CHF
  2. Nephrotic syndrome
  3. Liver disease
29
Q

What is pseudohyponatremia and what are it’s causes?

A

Isotonic hyponatremia - Normal amount of serum sodium, but increase in plasma solids (lipids, proteins) causes an artificial laboratory decrease in [sodium]

30
Q

What causes hypertonic hyponatremia? What are some examples? What are their treatments?

A

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
Q

What organ system is affected most by hyponatremia? What are the symptoms?

A

Neurological system due to cerebral edema

  • HA, delirium, irritability
  • muscle twitching, weakness
  • hyperactive DTR
32
Q 
What are symptoms of hyponatremia by organ system?
Neurological
CV
GI
GU
A 
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
Q

How is hypoNa diagnosed? How is it treated?

A

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
Q

What is the treatment in hypovolemic hypotonic hypoNa for the following Na levels?
Mild: 120-130
Moderate: 110-120
Severe: <110

A

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
Q

What are some causes of hypovolemic hyperNa (more water is lost compared to Na loss)? How is it treated?

A

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
Q

What are the causes of euvolemic hyperNa (Na stable, water lost)? How is it treated?

A
  • 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
Q

What are the causes of hypervolemic hyperNa (excess Na - rare)? How is it treated?

A
  • 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
Q

What are the clinical symptoms of hyperNa?

A

Neurological: AMS, restlessness, weakness, focal defects, confusion, seizures, coma
General: tissue and mucous membranes dry; decreased salivation

39
Q

How is hyperNa diagnosed?

A

Low urine volume

High urine osmolality >800

40
Q

What is used to differentiate between nephrogenic and central diabetes insipidus?

A

Desmopression

41
Q

What are the two different rules used in calculation of maintenance fluids?

A

100/50/20 rule: (first 10 kg100, second 10 kg50, 20/kg >20)/24
4/2/1 rule: 410kg + 210kg + 1*n/kg

42
Q

What are the (3) main things that affect Ca levels? In what ways?

A
  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
Q

What are the (3) hormones that affect calcium levels? How do they affect the levels of phosphorus?

A
  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
Q

What organ systems are acted upon in calcium and phosphorus homeostasis?

A

Bone
Kidneys
Gut

45
Q

What are (12) causes of hypoCa?

A
  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
Q

What are the organ systems affected by hypoCa? What are the symptoms?

A

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
Q

What happens to the levels of PO4 in the following conditions?
Renal insiffuciency
HypoPTH
Primary Vitamin D deficiency

A

Renal insufficiency: high
HypoPTH: high
Primary Vitamin D deficiency: low

48
Q 
What happens to the levels of PTH in the following conditions?
HypoPTH
Vitamin D deficiency
CKD
PseudohypoPTH
A

HypoPTH: low
Vitamin D deficiency: high
CKD: high
PseudohypoPTH: extremely high

49
Q 
What are the treatments for hypoCa?
Symptomatic
Long-term management
PTH deficiency
What additional electrlyte must also be corrected?
A

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
Q

What are the (4) main causes of hyperCa?

A
  1. Endocrinopathies
  2. Malignancies
  3. Pharmacologic
  4. Other
51
Q

What endocrinopathies may cause hyperCa? Why?

A

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
Q

What malignancies may lead to hyperCa? Why?

A

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
Q

What pharmacologic causes may lead to hyperCa? Why?

A
  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
Q

How do the following diseases cause hyperCa?
Sarcoidosis
Familial hypocalciuric hypercalcemia

A

Sarcoidosis - increased GI absorption

Familial hypocalciuric hypercalcemia

55
Q

What are the symptoms of hyperCa? (Hint: there is a mnemonic)

A

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
Q

What does an elevation in PTHrP indicate about the cause of hyperCa?

A

Likely due to malignancy

57
Q

What are the treatment options used in hyperCa? (Most cases only require treatment of underlying disease)

A
  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
Q

What is the risk of using phosphate replacement in patients with hyperCa?

A

Metastatic calcification

59
Q

Where does the majority of potassium excretion occur? What hormone plays an important role in its excretion?

A

Excretion occurs mostly in the kidneys (80%) through the levels of aldosterone. The rest is excreted through the GI system

60
Q

What are the main causes of hypoK in the following systems:
GI
Renal

A

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
Q

How does excess glucocorticoids cause hypoK?

A

Glucocorticoids exert mineralocorticoid action at high serum levels

62
Q

What is Bartter syndrome?

A

AR defect in salt reabsorption leading to increased renin levels, secondary ALD elevations, and chronic volume depletion

63
Q

What are non-GI or renal causes of hypoK?

A 
Low dietary intake
Insulin
Antibiotics - amphotericin B
Profuse sweating
Epinephrine (B2-agonists)

Medicine SHELF (13 decks)

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