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CPR II Exam 3 > Clinical Approach to Hyponatremia/Hypernatremia and Hypokalemia/Hyperkalemia (Selby) > Flashcards

Clinical Approach to Hyponatremia/Hypernatremia and Hypokalemia/Hyperkalemia (Selby) Flashcards

1
Q

What is hyponatremia defined as and what is the difference between mild, moderate, and severe forms?

Who is it commonly seen in?

A

Hyponatremia - serum sodium < 135 mEq/L

Mild - 130-134 mEq/L
Moderate - 120-129 mEq/L
Severe - < 120 mEq/L

  • more commonly seen in hospitalized pts, especially in the ICU, and less common in outpatients
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2
Q

What is the normal serum osmolarity in the body and what are the two systems that help regulate it?

What are the osmotic and non-osmotic stimuli that regulate ADH release?

A

Normal osmolarity = 280-290 mOsm/L
- serum osmolarity regulated by ADH and thirst mechanisms

ADH release due to:

  1. Osmotic Stimuli - inc. osmolarity detected by OSMORECEPTORS in anterior hypothalamus
  2. Non-osmotic Stimuli - dec. in BP or blood volume detected by arterial BARORECEPTORS
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3
Q

What are 4 additional Non-Osmotic Stimuli for ADH release (N/H/P/M)?

What are two medications that cause ADH release?

A
  • Nausea (vomiting = hypovolemia), Hypoxia, Pain (post-op pt.), and medications

Medications: opiates and antidepressants (SSRIs)

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4
Q

What is the primary cause of hyponatremia and what are two examples of it?

A
  • results primarily from increases in TOTAL BODY WATER (less from changes in total body sodium)

Increases in TBW occur due to:

  • excessive water intake (oral/IV)
  • dec. renal water excretion (can’t suppress ADH)
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5
Q

What is the time difference between Acute and Chronic Hyponatremia?

A 
Acute = < 48 hours
Chronic = > 48 hours

same time-frame for pts with HYPERnatremia

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6
Q

What is the stepwise approach to diagnosis of Hyponatermia?

When should labs be taken?

A
  1. Measure serum osmolarity
    • determine if hypotonic, isotonic, hypertonic hyponatremia
  2. if pt. has hypotonic hyponatremia, assess volume status
    • measure random urine sodium lvl
    • measure urine osmolarity

all labs need to be drawn at the SAME TIME - get plasma sodium, urine sodium, and urine osmolarity

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7
Q

What lab should be obtained if you suspect a patient has hyponatremia due to SIADH?

How is SIADH diagnosed and what are two main etiologies that must be ruled out?

A
  • get SERUM URIC ACID levels (will be LOW in SIADH)
    • inc. uric acid excretion in the urine
  • SIADH diagnosis is a diagnosis of EXCLUSION (should rule out other causes, like cortisol deficiency and hypothyroidism)
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8
Q

What is the stepwise process if a patient with hyponatremia is determined to be HYPOVOLEMIC?

A
  1. check urine osm > 300 mOsm/L
  2. check urine sodium lvls
  3. if > 20 mEq/L –> Renal Fluid Loss
    • diuretics, RTA, adrenal insufficiency, etc
  4. if < 20 mEq/L –> Extrarenal Fluid Loss
    • vomiting, diarrhea, 3rd spacing, blood loss, etc
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9
Q

What is the stepwise process if a patient with hyponatremia is determined to be EUVOLEMIC?

A
  1. check urine Osm lvls
  2. if urine osm < 100 mOsm/L = Primary Polydipsia
    • pt. drinking too much water –> STOP IT
  3. if urine osm > 300 mOsm/L –> check urine sodium
  4. if urine sodium > 20 mEq/L
    • SIADH, hypothyroidism, adrenal insufficiency, thiazide
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10
Q

What is the stepwise process if a patient with hyponatremia is determined to be HYPERVOLEMIC?

A
  1. check urine osm > 300 mOsm/L
  2. check urine sodium lvls
  3. if urine sodium < 20 mEq/L
    • nephrotic syndrome, heart failure, cirrhosis
  4. if urine sodium > 20 mEq/L
    • acute or chronic kidney failure (low GFR)
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11
Q

What are two common causes of SIADH?

A
  1. Small Cell Lung Carcinoma
    • most common malignancy associated with ectopic ADH production
  2. Postoperative state

many things can cause the development of SIADH

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12
Q

What are 6 drugs commonly associated with SIADH development?

A
  • antidepressants, anticonvulsants, antipsychotics, cyclophosphamide (ANTICANCER)
  • also opiates and MDMA (ecstasy)
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13
Q

What is the general rule of thumb for the treatment of Hyponatremia?

How should acute and chronic hyponatremia be treated?

What should SYMPTOMATIC patients receive?

A

Rule of Thumb: serum sodium should be corrected over the SAME TIME PERIOD it took to become low

Acute: rapid correction has little risk of osmotic demyelination syndrome (ODS)

Chronic: pt. at HIGH risk of developing ODS
- raise serum by 8-10 mEq/day with no more than 18 within first 48 hrs

Symptomatic: give HYPERTONIC SALINE (3%) to quickly raise sodium
- raise it enough so no longer symptomatic

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14
Q

What are common treatment options for hyponatremia caused by:

  1. Hypovolemic hyponatremia (2)
  2. Primary Polydipsia (Euvolemic)
  3. SIADH (3)
  4. Hypothyroidism
  5. Cortisol Deficiency
  6. Thiazides
  7. Hypervolemic hyponatremia (2)
A
  1. isotonic saline (no symptoms) and hypertonic saline (symptoms)
  2. water restriction and hypertonic saline (symptoms)
  3. water restriction, furosemide, salt/urea tablets
    • vaptans and demeclocycline
  4. thyroid replacement
  5. prednisone
  6. stop thiazides
    • *hypertonic saline for above 4 if symptoms**
  7. water restriction and furosemide
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15
Q

What are 4 common complications of Hyponatremia (S/C/D/ODS)?

A
  • seizures, coma, death, Osmotic Demyelination Syndrome (ODS - occurs with rapid Na correction)
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16
Q

Osmotic Demyelination Syndrome

When do symptoms manifest, what neurons are affected (2), and what is required for diagnosis?

A
  • symptoms occur 2-6 days after rapid Na correction (occurs in PONTINE and EXTRAPONTINE neurons)
  • symptoms are often irreversible or partially reversible (some pts. get “Locked-in” Syndrome where they are awake but cannot move)

Dx: head MRI (may take 4 wks to see changes)

too quick of correction causes brain cells to SHRINK, causing axonal shear damage as water enters extracellular space

17
Q

What is Hypernatremia and what two pt. populations are commonly affected?

What are 5 common risk factors for development and what is the most common cause of development?

A
  • defined as serum sodium > 145 mEq/L, typically seen in infants and the elderly (impaired thirst mechanism)

RF: trauma, burns, ICU pts, dementia, and uncontrolled diabetes

  • typically caused by unreplaced water loss (DEHYDRATION) and less commonly by Na overload
    • GI water loss (vomit/diarrhea), renal water loss, sweating, impaired thirst mechanism
18
Q

What does Hypernatremia result in and what clinical manifestations does it present with?

Which clinical manifestation is commonly seen in pediatric and neonate pts?

A
  • results in cellular shrinkage since there is an osmotic gradient for water to move out of cells into ECF
  • clinically manifests as NEUROLOGICAL symptoms (lethargy, seizures, irritability, altered mental status)
  • INTRACEREBRAL HEMORRHAGE more common in pediatric and neonate pts
19
Q

What is the 2 step approach to treating pts. with Hypernatremia?

How should Acute and Chronic Hypernatremia be treated?

A
  1. Replace the water deficit
    • 5% dextrose in water (D5W), hypotonic solutions
  2. correct underlying cause leading to water loss

Acute: can rapidly correct with little risk of cerebral edema

Chronic: pts. at inc. risk of cerebral edema
- goal: lower sodium by 10-12 mEq/L

20
Q

What is the primary regulator of serum potassium in the body?

What two cell types are responsible for secretion and reabsorption of potassium in this regulator?

A

THE KIDNEY (distal nephrons = urinary K secretion)

  • Principle Cells = K secretion
  • a-intercalated Cells = K reabsorption

Immediate Response: transcellular shift
Long-Term Response: renal excretion

21
Q

What is Hyperkalemia defined by?

What are 3 major clinical manifestations of Hyperkalemia?

A
  • Hyperkalemia = serum potassium > 5-5.5 mEq/L

C: cardiac arrhythmia (bradycardia), skeletal muscle weakness (diaphragm weakness), metabolic ACIDOSIS (dec. ammoniagenesis = dec. ammonium chloride excretion in kidneys)

22
Q

How do Hyperkalemia and Hypokalemia affect the resting membrane potential of skeletal muscle?

A

Hyperkalemia: makes membrane potential LESS negative

  • initially MORE excitable
  • long-term = Na channel inactivation = net dec. in membrane excitability (VENTRICULAR FIBRILLATION)

Hypokalemia: makes membrane potential MORE negative
- see U-WAVE on ECG and flat-inverted T-Waves

23
Q

What are the two main reasons that Hyperkalemia develops?

What should ALWAYS be reviewed in pts with Hyperkalemia?

A
  1. Transcellular Shift
    • pseudohyperkalemia, metabolic acidosis, meds, exercise, blood transfusion (K leaks out of RBCs), insulin deficiency (no Na/K ATPase stimulation), hyperglycemia/hyperosmolarity (water drags K out of cells)
  2. Decreased Renal Potassium Excretion
    • low aldosterone secretion (meds/adrenal insuff)
    • aldosterone resistance (K-sparing, Na Channel Block)
    • AKI/CKD (low GFR)

ALWAYS REVIEW medications of pts. with Hyperkalemia

24
Q

What is Pseudohyperkalemia and what are 3 things that can cause it? (R/S/L)

A
  • results from an artificial inc. in serum K due to K release from cells
    1. RBC hemolysis (mechanical trauma to cells)
  1. Serum Blood Samples (clotting = K out of platelets)
    • obtain plasma K to rule out thrombocytosis
  2. Leukocytosis (fragile WBCs in leukemia pts)
25
Q

How is Hyperkalemia diagnosed and what does Fractional Excretion of K (FEK) tell us?

What test should NOT be ordered for Hyperkalemic pts?

A
  • Dx based on HISTORY and EXAM (lab tests guided by suspected cause per history)
  • FEK: < 10% (Renal etiology) and > 10% (extrarenal etiology)
  • do NOT order Transtubular Potassium Gradient (TTKG) = Invalid test
26
Q

Hyperkalemia Treatment

What are 5 ways to treat patients?

A
  1. calcium gluconate if Peaked T-waves (stabilize cardiac membrane)
  2. Transcellular shift - insulin/dextrose, B2-agonists
  3. Potassium Removal - loop diuretic/thiazides, also exchange resins
  4. low potassium diet
  5. discontinue meds that increase potassium lvls
27
Q

Hyperkalemia and Exchange Resins

How do these resins work and where:

  1. Sodium Polystyrene Sulfonate
  2. Zirconium Cycloslicate
  3. Patiromer
A
  1. exchanges Na for potassium in COLON
  2. exchanges Na/H for potassium throughout INTESTINES
  3. exchanges Ca for potassium in COLON
28
Q

What is Hypokalemia and what are 3 risk factors for development?

What are 5 clinical manifestations of this condition? (CA/SM/R/MA/NDI)

A
  • Hypokalemia = serum potassium < 3.5 mEq/L

RF: diarrhea, vomiting, medications (diuretics/insulin)

C: cardiac arrhythmias, skeletal muscle weakness, rhabdomyolysis, metabolic ALKALOSIS, nephrogenic diabetes insipidus

29
Q

How are these causes of Hypokalemia caused:

  1. Transcellular Shift (inc. K uptake by cells) - 3
  2. Extrarenal Loss - 2
  3. Renal Loss - 3
A
  1. due to Insulin, B2-agonists, and metabolic ALKALOSIS
    • MOST COMMON reasons for shift
  2. GI Loss
    • Upper GI - vomiting, NG suction
    • Lower GI - diarrhea
    • cutaneous loss through SWEATING
  3. Diuretics (thiazide/loop), inc. mineralcorticoid activity (aldosterone inc. Na reabsorption), and Hypomagnesemia
30
Q

How is Hypokalemia diagnosed?

What are 2 Urinary Potassium Excretion tests that can be performed?

A
  • often clinically diagnosed through history and exam
    • laboratory test guided by these two processes
  1. 24 hr Urine Potassium Screen
    • BEST METHOD to assess renal K excretion
    • values > 25-30 mEq/L = renal K wasting
  2. Urine K/Cr ratio
    • Cr corrects for variation in urine volume
    • values > 13 mEq/g = renal K wasting (typically < 13 mEq/g is NORMAL)
31
Q

What are the 4 main treatments for Hypokalemia? (UC/RP/RM/RK)

A
  1. treat the underlying cause
  2. replace potassium deficit (Potassium Chloride)
    • K inc. by 0.1 mEq/L for every 10 mEq of KCl given
  3. replace magnesium if low
    • magnesium oxide or magnesium sulfate 1-2g IV
  4. repeat K to ensure it has normalized

CPR II Exam 3 (12 decks)

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