electrolyte imbalances Flashcards

1
Q

How do we maintain normal plasma osmolality: intake

A
  • Regulated by Osmoreceptors in Anterolateral Hypothalamus that detect Tonicity
  • Thirst response activated when Osmolality = 295 mOsm -> happens LATE
  • if pt is thristy at ER: really dehydrated
  • normal: 275-290
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2
Q

How do we maintain normal plasma osmolality: excretion

A
  • Regulated by Osmoreceptors that detect ADH & Tonicity
  • ADH is released when Osmolality = 280-290 mOsm
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3
Q

renal causes of hypovolemia vs extra-renal

A

renal:
- Diuretics
- Osmotic Diuresis
- Hypoaldosteronism
- Salt-wasting
- DI

extrarenal:
- GI loss
- skin loss: sweating
- respiratory
- hemorrhage: pure blood loss = water loss

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4
Q

osmolarity vs tonicity

A

Osmolarity: Objective, quantitative value that determines concentration
- what you measure in a test tube

Tonicity: Subjective, comparative value that assess movement of substance between two solutions separated by membrane
- is in relation between membrane and permeability

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5
Q

hypovolemia labs: urine Na+, osmolality, sp gravity

A

Urine Sodium:
- < 20 mM/L
- Due to increased sodium reabsorption to retain body fluid volumes

Urine Osmolality:
- >450 mOsm
- Due to decreased urine output

Urine Specific Gravity:
- 1.015
- Higher due to decreased urine output

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6
Q

Hypovolemia: the ECF is ________. list 3 categories/causes of hypovolemia

A

NORMAL OR EXPANDED ECF

Decreased CO: reduces circulating blood volume
- sepsis

Redistribution:
- Hypoalbuminemia: Decreased oncotic pressure = ↓ Intravascular Volume
- Capillary Leakage: Fluid seeping into interstitial spaces

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7
Q

hypovolemia labs: BUN:Cr

A

BUN: Cr
- normal: 10:1
- prerenal azotemia (decreased renal perfusion) + GI conditions: >20:1
- dehydration: 20:1

Urinary values:
- < 20
- >

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8
Q

hypovolemia tx:

A
  • Based on severity
  • Mild: Slow oral rehydration
  • IV fluids: based on electrolyte abnormality OR cause of hypovolemia (ie. active GI bleed)
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9
Q

Types of IV Fluids

A

Normal Saline: ECF replacement due to low osmotic pressure
- mostly distributed to INTERSTITIAL -> could cause third space

D5W: Maintenance fluid that is distributed throughout ALL compartments due to dextrose passing into all compartments

Fresh Frozen Plasma: Colloid that primarily stays intravascular

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10
Q

Hyponatremia: what are the sx dependent on

A

often associated with hypovolemia

dependent on :
- RATE of decrease: faster decline = more sx
- plasma level of sodium: really low Na+ = more sx

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11
Q

Hyponatremia: cycle of events in the brain

A

hypotonic state -> water gain causes excess water to move into the brain cells
- swelling: headache, nausea/vomit

rapid adaptation: brain cells respond by active transport to push electrolytes out of cells so water follows

slow adaption: loss of organic osmolytes

too rapid correction of hyponatremia = OSMOTIC DEMYELINATION
- damage to myelin; life threatening

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12
Q

Hyponatremia sx

A

mostly neurologic sx

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13
Q

Dx hyponatremia

A

Definition: plasma osmolality under 135
- normal: 135-145

other labs:
- Urine Osmolality
[Na+] Urine and [K+] Urine:
- Potassium is wanted to since both Na+ and K+ influence the body’s tonicity

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14
Q

hyponatremia with high plasma osmolality DDx

A
  • Hyperglycemia: uncontrolled DM
  • Mannitol

usually caused by the presence of other osmotically active substances in the blood that can draw water out of cells

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15
Q

hyponatremia with normal plasma osmolality DDx

A

occur in cases where there is an increase in other plasma components such as protein and lipids - > these conditions can affect the measurement of sodium

  • hyperproteinemia: multiple myeloma; neoplasms
  • hyperlipidemia
  • after bladder irrigation process
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16
Q

hyponatremia with low plasma osmolality DDx first steps

A

1) check urine osmolality: see if its excess water intake and assess kidney function

Urine osmolality < 100 mOsm:
- primary polydipsia
- osmostat error
- suggests that the kidneys are responding appropriately to the hyponatremia by excreting dilute urine

Urine osmolalilty > 100 mOsm:
- implies that the kidneys are still concentrating urine -> indicates body’s attempt to retain water
- check ECF volume status: ddx SIADH, heart, liver, kidney ds

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17
Q

hyponatremia + low plasma osmolality: Urine Osmolality > 100 mOsm; normal ECF

A
  • SIADH
  • Hypothyroidism
  • adrenal insufficiency
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18
Q

hyponatremia + low plasma osmolality: Urine Osmolality > 100 mOsm; increased ECF

A

conditions are often associated with edema and fluid overload

  • CHF
  • Cirrhosis
  • nephrotic syndrome
  • renal insufficiency
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19
Q

hyponatremia + low plasma osmolality: Urine Osmolality > 100 mOsm; decreased ECF

A

1) Check urinary Na+ concentration

urinary sodium (Na+) is less than 10:
- extra-renal loss: past vomiting and diuretic use

urinary sodium (Na+) is greater than 10:
- sodium wasting nephropathy
- hypoaldosteronism
- current diuretic use
- active vomiting

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20
Q

hyponatremia tx

A

Key in treatment is RATE of sodium infusion
- DO NOT CORRECT > 10-12 mM in first 24 hrs
- too quickly: rapid shift of sodium levels may destroy myelin sheath = Osmotic Demyelination

asymptomatic: 0.5-1.0 mM/hr

emergent sx:
- give hypertonic saline and increase 1-2 mmol/L for 3-4 h OR until sx improvement
- then: 0.5-1.0 mM/hr

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21
Q

Hypernatremia: s + s

A

Depends on Plasma Na+ levels and rate of Na+ decrease
- brain has mechanisms to protect ICF volume

-Mild: Thirst/Polyuria
- Moderate: Weakness
- Severe: Neurologic Deficits & Altered Mental Status
- Very Severe: Seizure & Coma

22
Q

Hypernatremia: what would you expect body to do

A

Renal: Kidneys will try to make maximally concentrated urine with minimal volume
- <500 mL/day
- >800 mOsm

Hypothalamus: THIRST response is activated to maintain adequate intake of free water

23
Q

Hypernatremia: treatment

A

Correct underlying cause

Correct water deficit:
- SLOW REHYDRATION- Risk of Osmotic Demyelination
- Plasma Sodium should decrease no more than 0.5 mM/hr or 12 mM/24 hours
- Enteral replacement is ideal

24
Q

Nephrogenic Diabetes Insipidus: definition and causes

A

Definition: Renal resistance to ADH

Inherited cause: Genetics

Acquired causes:
- Medications: Lithium (treatment for bipolar ds)
- Hypercalcemia
- Hypokalemia
- Pregnancy

25
Q

Central Diabetes Insipidus: definition and causes

A

Definition: Impairment of ADH secretion

Most common cause: Destruction of Pituitary
- Oftentimes nonreversible

26
Q

DI treatment: central vs nephrogenic

A

Central:
- intranasal desmopressin
- ADH secreting drugs
- low salt diet
- thiazide diuretics

Nephrogenic:
- treat underlying cause
- NSAIDS
- if taking lithium: amiloride
- low salt diet
- thiazide diuretics

27
Q

Hyper/Hypokalemia are assessed with fluid draws:

A

Venous blood *
Arterial Blood
Urine

Blood Draw Tips:
- Avoid drawing from a limb with an IV
- If must, draw the blood distal to IV site
- Use as large bore needle as possible to prevent hemolysis

28
Q

Potassium: GI system

A
  • we consume 40-120 mM per day and 90% is ABSORBED in GI
  • 10% GI loss: increased in renal failure and diarrhea
29
Q

Potassium summary

A

most abundant intracellular cation

  • ICF: ECF = 38:1
  • normal plasma: 3.5-5
  • normal intracellular: 150 avg (muscle cells have more)
  • normal extracellular: 30-70

Muscle has way more K+ in each cell
- Issue: pt that falls and rhabdo with crush injury -> can release LARGE AMOUNTS OF K+*****

30
Q
A
31
Q

Potassium: renal excretion

A
  • filtered K+: GFR x serum potassium concentration
  • passive reabsorption (90%): proximal convoluted tubule and loop of henle
  • active secretion: distal convoluted tubule and collecting ducts by PRINCIPAL CELLS
  • secretion and reabsorption rates change based on K+ concentration and ALDOSTERONE
32
Q

How to insulin and Beta 2 agonists affect K+ levels?

A

Insulin:
- directly and indirectly increases K+ levels through Na+-K+ ATPase

β2 Agonists:
- stimulates Na+-K+ ATPase = ↑ ICF K+

33
Q

What increases or decreases Na/K ATPase

A

Increase: higher intracellular Na+

Decrease:
- digoxin toxicity
- CHF
- Chronic renal failure

34
Q

Hyperkalemia: decreased K+ excretion causes

A
  • renal failure
  • interstitial nephritis
  • sickle cell ds
  • hypoaldosteronism
  • durgs: ACEi, trimethoprim, NSAIDs, spironolactone, triamterene
35
Q

Hyperkalemia: potassium shift causes

A

Rhabdomyolysis & Hemolysis = Release of ICF K+**
Exercise**
- more exercise = more K+ release
- strenuous + beta blocker: UP TO 4 mmmol/L -> need cardiac rehab

others:
- burns
- sepsis
- hypertonicity
- insulin deficiency
- metabolic acidosis
- drugs: digoxin, beta blockers, succinylcholine, arginine

36
Q

hyperkalemia sx

A

Often asymptomatic

If symptomatic:
- MSK: Weakness; K = muscle issues
- Cardio: Palpitations
- GI: Constipation

37
Q

hyperkalemia tx - acute

A

Treat underlying cause! - HOWEVER: do not delay treatment to find the cause

As opposed to Sodium, MUST have rapid correction of K+
- Due to risk of Cardiac Abnormalities

acute tx:
- calcium gluconate
- glucose and insulin
- albuterol
- diuretics
- kayexalate
- hemodialysis

38
Q

hyperkalemia labs + dx

A

Dx: serum K+ > 5

others:
- BUN/Cr: Determine if renal
- Serum glucose
- EKG: PEAKED t waves
- Urinalysis

39
Q

hyperkalemia tx - chronic

A

Dietary Restriction
Removal of Iatrogenic cause
Loop Diuretics
Treat underlying cause:
- ex: Fludrocortisone for hypoaldosteronism

40
Q

hypokalemia: causes

A
  • renal potassium loss
  • potassium shift into ICF
  • decreased K+ intake
  • extrarenal potassium loss
  • sample error
41
Q

hypokalemia: causes of renal potassium loss

A

Excess Aldosterone:
- Hyperaldosteronism
- Cushings
- Renovascular HTN

↑ Renal Flow at distal nephron:
- Diuretics
Hypomagnesemia: Mg2+ is needed to transport K+

Renal Tubular Acidosis

Genetic Disorder
- Bartter’s Syndrome
- Liddle’s Syndrome

42
Q

hypokalemia: causes of K+ shift into the cell

A
  • excess insulin
  • alkalosis
  • beta adrenergic excess
  • hypokalemic periodic paralysis
43
Q

hypokalemia: extrarenal loss causes

A
  • vomit/diarrhea
  • villous adenoma
  • zollinger-ellison syndrome
44
Q

hypokalemia sx

A

May be asymptomatic

If Symptomatic:
- Muscle cramps
- Fatigue
- Weakness
- Constipation

45
Q

hypokalemia signs

A

If Diuretics = ↓ BP
If Gitelman’s Syndrome = ↓ BP
If Hyperaldosteronism = ↑ BP
Irregular HR
Paralysis
Decreased bowel sounds

46
Q

Serum K+ < 3.5 mM

what other labs/tests to check to help with dx and tx?

A

hypokalemia

BUN:Cr: To assess renal function
Glucose
Magnesium
EKG: Presence of U WAVES
ABG

47
Q

hypokalemia tx: who do you give potassium supplements to

A

Stable: Treat underlying cause; low Na+ diet, d/c meds

Potassium replacement:
- Intolerant to low Na+ diet
- Pt with nausea, vomiting, diarrhea
- Pt unable to stop Diuretics or Laxatives
- Pt with drug-induced hypokalemia

48
Q

24-Hr Urine: hypokalemia results

A

If [K+]Urine < 30 mM = Extrarenal
[K+]Urine > 30 mM = Renal

49
Q

Potassium Replacement

A

in general: 40-100 mmol/day = effective
- Oral Replacement is preferred

if IV:
- K+ suspended in NS
- No faster than 40 mM/hr -> faster will cause cardiac arrest, K+ is irritating and pts will complain that it is burning
- If 20-40 mM/hr, MUST monitor cardiac

50
Q

Magnesium replacement in hypokalemia

A

only indicated if hypokalemia is refractory to tx AND:
- CHF
- Chemo (cisplatin)
- digoxin toxicity
- loop diuretics

51
Q

hypokalemia f/u

A

Emergency: check electrolytes every 1-2 h

Stable: check 4-6h after tx; check daily

Outpatient setting: check weekly until stable; then check monthly or quarterly depending on pt compliance