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CPR II Exam #2 > Approach to Fatigue and Generalized Weakness > Flashcards

Approach to Fatigue and Generalized Weakness Flashcards

1
Q

Normal serum Osm:

Regulated by which 2 systems:

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

A

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.

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2
Q

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

A 
Nausea
Hypoxia
Pain
Meds: opiates, anti-psychotics, anti-depressants (SSRIs)
Pregnancy
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3
Q

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

What causes it?

A

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

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

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4
Q

What can increase TBW? (2)

A

Excessive water intake

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

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5
Q

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

A
  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.
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6
Q

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

A

Serum uric acid (low serum uric acid is associated)

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7
Q

What is iso-osmotic hyponatremia?

What causes it?

A

Hyponatremia with normal serum Osm.

Usually a lab error.

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8
Q

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

A

Hypovolemic: decreased TBW, decreased [Na+]

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

Hypervolemic: increased TBW, increased [Na+]

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9
Q

What is the correction for hyperglycemia sodium levels?

A

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

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10
Q

What are some causes for hyperosmotic hyponatremia?

A

Hyperglycemia

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

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11
Q

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

A

Cortisol deficiency - measure cortisol

Hypothyroidism - measure TSH

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12
Q

What cancer is the most common malignancy associated with SIADH?

A

Small cell lung cancer

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13
Q

What drugs are associated with SIADH? (6)

A

Anti-depressants
Anti-convulsants
Anti-psychotics

Cyclophosphamide
Opiates
MDMA (Ecstasy)

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14
Q

At what point do people with hyponatremia become symptomatic?

What are the symptoms?

Complications include: (3)

A

[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)

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15
Q

What is the general rule of thumb for treating hyponatremia?

A

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

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16
Q

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

A

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

Ch. - Yes

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17
Q

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

A

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

18
Q

What is the treatment for symptomatic patients with hyponatremia?

A

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

Give hypertonic saline (3%) continuous infusion.

19
Q

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

A 
Isotonic saline (no SX)
Hypertonic saline (w/ SX)
20
Q

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

A

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

21
Q

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

A

Water restriction

Furosemide

22
Q

When do clinical manifestations of ODS begin?

Where does the demyelination occur?

SX:

How is it Dx?

A

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.

23
Q

How does the demyelination occur in OCS?

A

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

24
Q

How is [K+] adjusted immediately?

How is it adjusted long-term?

A

Transcellular shift

Renal excretion

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

25
Q

What cells within the nephron regulate secretion of K+?

A 
Principal cells (secretion)
a-intercalated cells (reabsorption)

Both in distal parts of nephron

26
Q

What unique transporters exist in the:

TAL
CD principal cell
CD intercalated cell

A

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

27
Q

3 major clinical manifestations of hyperkalemia

A

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

28
Q

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

A

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.)

29
Q

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)?

A

Peaked T waves

Flattened P waves, prolonged PR interval, prolonged QRS, continued peaking of T waves.

Sinusoid pattern -> VFib

30
Q

2 main reasons for hyperkalemia

A 
Transcellular shift (increased K+ release from cells)
Decreased renal K+ excretion
31
Q

Causes of transcellular shift (7)

A 
Pseudohyperkalemia
Metabolic acidosis
Insulin abnormalities
Increased tissue catabolism
Meds
Exercise
Blood transfusions
32
Q

Causes of decreased renal K+ excretion (6)

A 
Low aldosterone secretion
Aldosterone resistance
AKI/CKD
Hypovolemia
Ureterojejunostomy
Intrinsic renal defect - rare
33
Q

Pseudohyperkalemia is cause by: (3)

A

Artificial increase in serum [K+] due to K+ release from cells due to:

  • RBS hemolysis
  • Serum blood samples
  • Leukocytosis
34
Q

Dx of Hyperkalemia (3)

A

Usually a clinical Dx based on Hx and exam

Labs

Fractional excretion of K+ (FEK): <10% indicates renal etiology, >10% indicates an extrarenal etiology

35
Q

Hyperkalemia Tx for:

Peaked T waves (1)
Transcellular shift (3)
K+ removal (2)

A

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

36
Q

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

A

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

37
Q

Apnea vs. Hypopnea

A

Apnea - cessation of airflow for 10 sec.

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

38
Q

AHI for Dx (mild, moderate, severe)

AHI for Dx in patients with CVD

A

5-14 is mild
15-29 is moderate
>30 is severe

AHI > 5 if w/ CVD

39
Q

Systolic HF EF:

Diastolic HF EF:

A

Systolic: EF < 40%

Diastolic: EF > 40% (EF is OK)

40
Q

NYHA classification of HF classes I-IV

A

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

CPR II Exam #2 (20 decks)

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