Approach to Fatigue and Generalized Weakness

Question 1

Normal serum Osm:

Regulated by which 2 systems:

ADH is released in response to osmotic and non-osmotic stimuli. What are they?

Answer 1

280-290 mOsm/kg

ADH, thirst system

Osm: increased serum Osm detected by osmoreceptors in anterior hypothalamus.
Non-osmotic: from decreases in BP or BV detected by baroreceptors.

Question 2

What are some non-osmotic stimuli for ADH release? (5)

Answer 2

Nausea
Hypoxia
Pain
Meds: opiates, anti-psychotics, anti-depressants (SSRIs)
Pregnancy

Question 3

Hyponatremia is defined by a Na+ level of:
What is severe hyponatremia?

What causes it?

Answer 3

<135 mEq/L
Severe - <120 mEq/L

Increases in TBW; less from changes in actual [Na+].

Question 4

What can increase TBW? (2)

Answer 4

Excessive water intake

Decreased renal excretion of water - usually from inability to suppress ADH release

Question 5

What is the systematic diagnostic approach to hyponatremia? (3)

Answer 5

1. Measure serum Osm: determine if hypo, iso, hyperosmotic hyponatremia.
2. If hypo-osmotic hyponatremia, assess volume status of patient: hypovolemic, euvolemic, hypervolemic, etc.
3. If hypo-osmotic hyponatremia, measure random urine Na+ level and urine Osm: will help differentiate etiology of hypo-osmotic.

Question 6

After the systematic diagnostic approach to hyponatremia, if you suspect SIADH, what should you measure?

Answer 6

Serum uric acid (low serum uric acid is associated)

Question 7

What is iso-osmotic hyponatremia?

What causes it?

Answer 7

Hyponatremia with normal serum Osm.

Usually a lab error.

Question 8

Hypo-osmotic hyponatremia is divided into 3 subtypes based on ECF volumes. What are they and how are they diagnosed?

Answer 8

Hypovolemic: decreased TBW, decreased [Na+]

Euvolemic: increased TBW, no change in [Na+]

Hypervolemic: increased TBW, increased [Na+]

Question 9

What is the correction for hyperglycemia sodium levels?

Answer 9

Na+ decreases by 1.6 mEq/L for every 100 mg/dL increase in Glc

Question 10

What are some causes for hyperosmotic hyponatremia?

Answer 10

Hyperglycemia

Hypertonic infusions: glc, glycerol, mannitol, sorbitol, etc.

Question 11

SIADH is a Dx of exclusion, but first, what 2 things must be ruled out?

Answer 11

Cortisol deficiency - measure cortisol

Hypothyroidism - measure TSH

Question 12

What cancer is the most common malignancy associated with SIADH?

Answer 12

Small cell lung cancer

Question 13

What drugs are associated with SIADH? (6)

Answer 13

Anti-depressants
Anti-convulsants
Anti-psychotics

Cyclophosphamide
Opiates
MDMA (Ecstasy)

Question 14

At what point do people with hyponatremia become symptomatic?

What are the symptoms?

Complications include: (3)

Answer 14

[serum Na+] < 125 mEq/L

HA, fatugue, dizziness, nausea, confusion, etc.

Falls/fx, death, Osmotic demyelination syndrome (from rapid serum Na+ correction in chronic hyponatremia)

Question 15

What is the general rule of thumb for treating hyponatremia?

Answer 15

Serum Na+ should be corrected over the same period of time it took to become low.

Question 16

Are patients with acute hyponatremia (<48 hrs) at risk for ODS? Can patients with chronic hyponatremia (>48 hrs or unknown duration)?

Answer 16

Ac. - No, because they can have rapid changes in serum Na+

Ch. - Yes

Question 17

What is the goal when raising serum Na+ in a patient with chronic hyponatremia?

Answer 17

Raise serum Na+ by 8-10 mEq/day with no more than 18 mEq/L in first 48 hrs.

Question 18

What is the treatment for symptomatic patients with hyponatremia?

Answer 18

Give 100 mL bolus of hypertonic saline (3%) over 10 min. Repeat is SX continue up to 3x.

Give hypertonic saline (3%) continuous infusion.

Question 19

What is the treatment for patients with hypovolemic hypo-osmotic hyponatremia? (2)

Answer 19

Isotonic saline (no SX)
Hypertonic saline (w/ SX)

Question 20

What is the treatment for patients with euvolemic hypo-osmotic hyponatremia? (4)

Answer 20

Water restriction
Hypertonic saline (w/ SX)
Furosemide
Salt or urea tabs

Question 21

What is given for treatment in patients with hypervolemic hypo-osmotic hyponatremia? (2)

Answer 21

Water restriction

Furosemide

Question 22

When do clinical manifestations of ODS begin?

Where does the demyelination occur?

SX:

How is it Dx?

Answer 22

2-6 days post rapid Na+ correction

Pontine and extrapontine neurons

Dysarthria, dysphagia, seizures, lethargy, coma (some will have Locked-in syndrome - awake but unable to move), death.

Head MRI, but may take up to 4 wks to be able to see.

Question 23

How does the demyelination occur in OCS?

Answer 23

Increased Na+ leads to water loss from neurons which leads to axon damage and disruption of BBB

Question 24

How is [K+] adjusted immediately?

How is it adjusted long-term?

Answer 24

Transcellular shift

Renal excretion

Total [K+] in the body is determined by kidneys

Question 25

What cells within the nephron regulate secretion of K+?

Answer 25

``` Principal cells (secretion) a-intercalated cells (reabsorption) ``` Both in distal parts of nephron

Question 26

What unique transporters exist in the: TAL CD principal cell CD intercalated cell

Answer 26

TAL: Na+K+Cl-2 CD principal cell: ENaC (acted on by aldosterone) CD intercalated cell: K+/H+ anti-porter

Question 27

3 major clinical manifestations of hyperkalemia

Answer 27

Cardiac arrhythmias Skeletal m. weakness Metabolic acidosis (decreased ammonium excretion in kidneys)

Question 28

What is the effect of high [K+] on membrane potential?

Answer 28

Membrane potential becomes less negative (increases) which makes firing an AP easier initially. Long-term, these channels can become inactivated and lead to a net decrease in membrane excitability (cardiac conduction problems, weakness, etc.)

Question 29

What are the ECG changes seen in mildly elevated (6-7) hyperkalemia? As hyperkalemia worsens, what else is seen? (4) What is seen in severe hyperkalemia (>9)?

Answer 29

Peaked T waves Flattened P waves, prolonged PR interval, prolonged QRS, continued peaking of T waves. Sinusoid pattern -> VFib

Question 30

2 main reasons for hyperkalemia

Answer 30

``` Transcellular shift (increased K+ release from cells) Decreased renal K+ excretion ```

Question 31

Causes of transcellular shift (7)

Answer 31

``` Pseudohyperkalemia Metabolic acidosis Insulin abnormalities Increased tissue catabolism Meds Exercise Blood transfusions ```

Question 32

Causes of decreased renal K+ excretion (6)

Answer 32

``` Low aldosterone secretion Aldosterone resistance AKI/CKD Hypovolemia Ureterojejunostomy Intrinsic renal defect - rare ```

Question 33

Pseudohyperkalemia is cause by: (3)

Answer 33

Artificial increase in serum [K+] due to K+ release from cells due to: - RBS hemolysis - Serum blood samples - Leukocytosis

Question 34

Dx of Hyperkalemia (3)

Answer 34

Usually a clinical Dx based on Hx and exam Labs Fractional excretion of K+ (FEK): <10% indicates renal etiology, >10% indicates an extrarenal etiology

Question 35

Hyperkalemia Tx for: Peaked T waves (1) Transcellular shift (3) K+ removal (2)

Answer 35

Peaked T waves - Calcium gluconate Transcellular shift - insulin/dextrose, B2 agonist, Bicarb infusion K+ removal - Loop diuretics or thiazide, Exchange resins Also can reduce K+ in diet or D/C meds that are contributing

Question 36

What is the main Exchange resin used for K+ removal?

Answer 36

Sodium polystryene sulfonate (Kayexalate) - exchange Na+ for K+ in the colon

Question 37

Apnea vs. Hypopnea

Answer 37

Apnea - cessation of airflow for 10 sec. | Hypopnea - reduction of airflow for 10 sec. w/ >3% oxygen desats.

Question 38

AHI for Dx (mild, moderate, severe) AHI for Dx in patients with CVD

Answer 38

5-14 is mild 15-29 is moderate >30 is severe AHI > 5 if w/ CVD

Question 39

Systolic HF EF: Diastolic HF EF:

Answer 39

Systolic: EF < 40% Diastolic: EF > 40% (EF is OK)

Question 40

NYHA classification of HF classes I-IV

Answer 40

I - ASX II - minor SX w/ modest exertion III - moderate SX w/ minor exertion IV - SX at rest