Approach to Fatigue and Generalized Weakness Flashcards
Normal serum Osm:
Regulated by which 2 systems:
ADH is released in response to osmotic and non-osmotic stimuli. What are they?
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.
What are some non-osmotic stimuli for ADH release? (5)
Nausea Hypoxia Pain Meds: opiates, anti-psychotics, anti-depressants (SSRIs) Pregnancy
Hyponatremia is defined by a Na+ level of:
What is severe hyponatremia?
What causes it?
<135 mEq/L
Severe - <120 mEq/L
Increases in TBW; less from changes in actual [Na+].
What can increase TBW? (2)
Excessive water intake
Decreased renal excretion of water - usually from inability to suppress ADH release
What is the systematic diagnostic approach to hyponatremia? (3)
- Measure serum Osm: determine if hypo, iso, hyperosmotic hyponatremia.
- If hypo-osmotic hyponatremia, assess volume status of patient: hypovolemic, euvolemic, hypervolemic, etc.
- If hypo-osmotic hyponatremia, measure random urine Na+ level and urine Osm: will help differentiate etiology of hypo-osmotic.
After the systematic diagnostic approach to hyponatremia, if you suspect SIADH, what should you measure?
Serum uric acid (low serum uric acid is associated)
What is iso-osmotic hyponatremia?
What causes it?
Hyponatremia with normal serum Osm.
Usually a lab error.
Hypo-osmotic hyponatremia is divided into 3 subtypes based on ECF volumes. What are they and how are they diagnosed?
Hypovolemic: decreased TBW, decreased [Na+]
Euvolemic: increased TBW, no change in [Na+]
Hypervolemic: increased TBW, increased [Na+]
What is the correction for hyperglycemia sodium levels?
Na+ decreases by 1.6 mEq/L for every 100 mg/dL increase in Glc
What are some causes for hyperosmotic hyponatremia?
Hyperglycemia
Hypertonic infusions: glc, glycerol, mannitol, sorbitol, etc.
SIADH is a Dx of exclusion, but first, what 2 things must be ruled out?
Cortisol deficiency - measure cortisol
Hypothyroidism - measure TSH
What cancer is the most common malignancy associated with SIADH?
Small cell lung cancer
What drugs are associated with SIADH? (6)
Anti-depressants
Anti-convulsants
Anti-psychotics
Cyclophosphamide
Opiates
MDMA (Ecstasy)
At what point do people with hyponatremia become symptomatic?
What are the symptoms?
Complications include: (3)
[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)
What is the general rule of thumb for treating hyponatremia?
Serum Na+ should be corrected over the same period of time it took to become low.
Are patients with acute hyponatremia (<48 hrs) at risk for ODS? Can patients with chronic hyponatremia (>48 hrs or unknown duration)?
Ac. - No, because they can have rapid changes in serum Na+
Ch. - Yes
What is the goal when raising serum Na+ in a patient with chronic hyponatremia?
Raise serum Na+ by 8-10 mEq/day with no more than 18 mEq/L in first 48 hrs.
What is the treatment for symptomatic patients with hyponatremia?
Give 100 mL bolus of hypertonic saline (3%) over 10 min. Repeat is SX continue up to 3x.
Give hypertonic saline (3%) continuous infusion.
What is the treatment for patients with hypovolemic hypo-osmotic hyponatremia? (2)
Isotonic saline (no SX) Hypertonic saline (w/ SX)
What is the treatment for patients with euvolemic hypo-osmotic hyponatremia? (4)
Water restriction
Hypertonic saline (w/ SX)
Furosemide
Salt or urea tabs
What is given for treatment in patients with hypervolemic hypo-osmotic hyponatremia? (2)
Water restriction
Furosemide
When do clinical manifestations of ODS begin?
Where does the demyelination occur?
SX:
How is it Dx?
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.
How does the demyelination occur in OCS?
Increased Na+ leads to water loss from neurons which leads to axon damage and disruption of BBB
How is [K+] adjusted immediately?
How is it adjusted long-term?
Transcellular shift
Renal excretion
Total [K+] in the body is determined by kidneys
What cells within the nephron regulate secretion of K+?
Principal cells (secretion) a-intercalated cells (reabsorption)
Both in distal parts of nephron
What unique transporters exist in the:
TAL
CD principal cell
CD intercalated cell
TAL: Na+K+Cl-2
CD principal cell: ENaC (acted on by aldosterone)
CD intercalated cell: K+/H+ anti-porter
3 major clinical manifestations of hyperkalemia
Cardiac arrhythmias
Skeletal m. weakness
Metabolic acidosis (decreased ammonium excretion in kidneys)
What is the effect of high [K+] on membrane potential?
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.)
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)?
Peaked T waves
Flattened P waves, prolonged PR interval, prolonged QRS, continued peaking of T waves.
Sinusoid pattern -> VFib
2 main reasons for hyperkalemia
Transcellular shift (increased K+ release from cells) Decreased renal K+ excretion
Causes of transcellular shift (7)
Pseudohyperkalemia Metabolic acidosis Insulin abnormalities Increased tissue catabolism Meds Exercise Blood transfusions
Causes of decreased renal K+ excretion (6)
Low aldosterone secretion Aldosterone resistance AKI/CKD Hypovolemia Ureterojejunostomy Intrinsic renal defect - rare
Pseudohyperkalemia is cause by: (3)
Artificial increase in serum [K+] due to K+ release from cells due to:
- RBS hemolysis
- Serum blood samples
- Leukocytosis
Dx of Hyperkalemia (3)
Usually a clinical Dx based on Hx and exam
Labs
Fractional excretion of K+ (FEK): <10% indicates renal etiology, >10% indicates an extrarenal etiology
Hyperkalemia Tx for:
Peaked T waves (1)
Transcellular shift (3)
K+ removal (2)
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
What is the main Exchange resin used for K+ removal?
Sodium polystryene sulfonate (Kayexalate) - exchange Na+ for K+ in the colon
Apnea vs. Hypopnea
Apnea - cessation of airflow for 10 sec.
Hypopnea - reduction of airflow for 10 sec. w/ >3% oxygen desats.
AHI for Dx (mild, moderate, severe)
AHI for Dx in patients with CVD
5-14 is mild
15-29 is moderate
>30 is severe
AHI > 5 if w/ CVD
Systolic HF EF:
Diastolic HF EF:
Systolic: EF < 40%
Diastolic: EF > 40% (EF is OK)
NYHA classification of HF classes I-IV
I - ASX
II - minor SX w/ modest exertion
III - moderate SX w/ minor exertion
IV - SX at rest
