1
Q
Evaluation of Hyponatremia
- After initial steps of a thorough H&P, evaluate fluid status and then get which 4 labs first?
- Which 2 labs second?
A
- 1st: UA sodium, UA osmolality, serum osmolality, CMP
- 2nd: TSH, serum cortisol
2
Q
Tx of Hyponatremia
- If Na is <125 or symptomatic, what is the tx?
- ___ hyponatremia must be managed w/ extreme care
- Rapid increase in serum sodium can lead to _______
- Use of _____ is reserved for severe symptomatic cases
- What is the “traditional” treatment of chronic hyponatremia? to induce what?
- _____ are a newer class of tx agents which are vasopressin receptor antagonists
A
- Hospitalize!
- Chronic
- Cerebral pontine myelinolysis (CPM)
- Hypertonic solutions (3% NaCl)
- Demeclocycline / to induce nephrogenic diabetes insipidus
- “Vaptans”
3
Q
Tx of Hyponatremia
- In pts w/ severe symptomatic hyponatremia, the rate of sodium correction should be ____ in the first 24 hrs and ___ or less in 48 hours.
- ****If CHRONIC hyponatremia, should try to keep it ___ or less in the first 24 hours*****
A
- 6-12 mEq/L
- 18 mEq/L
- 8 mEq/L
4
Q
When correcting Hyponatremia, how often should you be checking serum sodium as you are replacing it (to make sure not overcorrecting)?
A
q2h
5
Q
- Poorly understood entity characterized by focal demyelination in the pons and extra-pontine areas
- Is it reversible?
- Dysarthria, dysphagia, seizures, AMS, quadriparesis, hypotension begin ___ after over-correction of hyponatremia
A
Central Pontine Myelinolysis (CPM)
- Irreversible
- 1-3 days after
6
Q
Which condition?
- A hypertonic disorder due to serum sodium >145 mEqL
- “Too little water relative to salt”
- Clinical features due to brain shrinkage secondary to increased ECF osmolality
A
Hypernatremia
7
Q
3 causes of Hypernatremia
A
- Too little dietary water
- Too much dietary salt
- Excessive water loss from the body
8
Q
4 causes of Hypernatremia
A
- GI losses: elderly / infants w/ diarrhea
- Skin loss: sweating, fever
- Renal loss
- Drug related: diuretics, lithium (can induce nephrogenic diabetes insipidus)
9
Q
Clinical features of what condition?
- Often asymptomatic
- Thirst
- AMS / weakness
- Neuromuscular irritability
- Focal neurologic deficits
- Seizures or coma
A
Hypernatremia
10
Q
Symptoms of Hypernatremia are related to rate of onset. If hypernatremia develops slowly, sxs will be ____.
A
Less dramatic
11
Q
Normal Response to Hypernatremia
- In response to hypernatremia, the body’s homeostatic mechanisms will normally do what 2 things?
- The vast majority of cases of hypernatremia are due to _____.
A
- Create thirst / increase fluid intake
- Maximally concentrate urine to prevent further water loss
- Water loss (GI tract, skin, renal)
12
Q
Which condition?
- Non-osmotic urinary water loss in setting of elevated serum sodium: urine is dilute when it should be concentrated (the collecting ducts are impermeable to water - water is not reabsorbed)
A
Diabetes Insipidus
13
Q
Which type of diabetes insipidus?
- Due to impaired secretion of antidiuretic hormone (ADH)
- Also called _____.
- Typically treated w/ _____
A
- Central DI
- Neurogenic DI
- Desmopressin (often an inhaled dDAVP nasal spray or IV DDAVP)
14
Q
Which type of diabetes insipidus?
- Lack of kidney response to ADH, causing continued water loss even though patient is low on water.
- Adequate ADH is present
A
Nephrogenic DI
15
Q
Nephrogenic Diabetes Insipidus can be genetic or acquired.
- Acquired is typically from which 4 things?
- What is the treatment?
A
- Chronic renal insufficiency
- Tubulointerstitial renal disease
- Amyloidosis
- Lithium toxicity
Tx:
- Thiazide diuretic
- Amiloride (K sparing diuretic)
- Chlorpropamide (antidiabetic oral agent)
- NSAIDs have been tried (including Indomethacin)
16
Q
Tx of Hypernatremia
- ____ if severe
- Stop water loss
- Replace water deficit in what 3 ways? w/ what fluid?
- Do not replace too rapidly, especially is the hypernatremia is _____. Why?
- It is okay to correct rapidy if what?
A
- Hospitalize
- Oral, NG tube, IV w/ hypotonic fluids
- present for several days (can cause seizures, brain damage, CPM)
- Tx Rapid: If hypernatremia developed acutely
17
Q
In order to replace free water in hypernatremia, you need to calculate what?
A
Water deficit
18
Q
- Major intracellular cation
- Renal excretion is the major route of elimination
- Regulation of renal ___ excretion and total body ___ balance occurs in the distal nephron
- Aldosterone causes increased renal excretion
A
Serum Potassium
19
Q
Which condition?
- Nearly 98% of body’s K is intracellular
- Total body K stores of approximately 50 mEq/kg
- 20% of hospitalized pts are _____
- 80% of pts who are receiving diuretics become ____.
A
Hypokalemia
20
Q
Clinical presentation of which condition?
- Weakness, fatigue
- Muscle cramps
- Hyporeflexia
- Flaccid paralysis (ascending)
- Hypercapnia
- Which one is most important (not listed here)****
A
Hypokalemia
- Cardiac arrhythmias
21
Q
T/F
- K can be replaced more rapidly than Na
A
True
22
Q
4 ECG findings of Hypokalemia
A
- Flattened T waves
- Prominent U waves
- Premature Ventricular Contractions (PVC’s)
- Depressed ST segments
23
Q
Hypokalemia mnemonic
hYpOkalemia U CRAMP
A
- U waves
- Cramping
- Resp failure / rhabdomyolysis
- Anorexia, N/V
- Muscle weakness
- Paralysis
24
Q
3 mechanisms which cause Hypokalemia
A
- Transcellular shifts
- Renal losses
- Extrarenal losses
25
**Which mechanism causing Hypokalemia?**
* Drugs: insulin, caffeine, bronchodilators, theophylline
* Delirium tremens
* Hyperthyroidism
* Metabolic alkalosis
(all lead to increase beta-adrenergic activity which causes K to shift \_\_\_\_\_)
**Transcellular Shifts**
* K shifts out of blood stream and into the cells
26
**Renal Losses causing Hypokalemia**
* ___ are the most common cause
* Aldosterone facilitates K excretion in the _____ therefore, high aldosterone states such as Hyperaldosteronism and Cushing's can lead to hypokalemia
* Renal tubular acidosis types 1&2
* Diuretics
* distal tubules
27
* What are 3 extrarenal losses causing Hypokalemia?
* Which one causes metabolic alkalosis, which further promotes renal potassium loss?\*
* Vomiting & diarrhea
* Burns
* Magnesium deficiency
* \*vomiting, NG suction
28
**Tx of Hypokalemia**
* Replace K and if possible tx underlying cause
* ___ monitoring if inpatient
* ____ replacement is preferred method
* IV reserved for those not able to eat
* If giving IV potassium via peripheral IV (not central line), include ____ with it because why?
* Never ____ IV potassium!!
* Telemetry
* Oral potassium (better absorption)
* Lidocaine, it burns and can destroy veins
* Push, should be given slowly
29
**How do you replace potassium?**
* For every 0.1 mEq/L below 4mEq/L, give ___ mEq/L
10
30
**Special Circumstances of Tx of Hypokalemia**
* ______ is important in potassium reuptake, and if low can hinder replacement of potassium
* draw Mg if hypokalemia is severe/resistant
* Hypokalemia precipitates ____ toxicity
* Hypomagnesemia
* Digoxin
31
**Which condition?**
* In absence of renal failure or other identifiable causes, is actually quite rare
* Relatively asymptomatic
* Muscle weakness
* begins in legs, acsends to trunk/arms
* "ascending flaccid paralysis"
* _ECG changes show what?_
**Hyperkalemia**
* Potentially life threatening arrhythmias
* Seen in 50% of patients
* _Peaked T waves\*\*_
* Widened QRS
* Junctional rhythm
* Ventricular fibrillation
32
Mnemonic for Hyperkalemia
"A FACT"
* Arrhythmias
* Flaccid paralysis
* Ascending muscle weakness
* Conduction abnormalities
* T waves
33
2 "factitious" causes of Hyperkalemia (Pseudohyperkalemia)
* Hemolysis
* Repeated fist clenching w/ tourniquet in place (poor venipuncture technique)
34
3 causes of Hyperkalemia from Impaired K excretion
* **Renal failure**
* **Mineralocorticoid deficiency**
* Addison's Disease
* Hypoaldosteronism
* **Renal tubular dysfunction**
35
5 drugs which can cause Hyperkalemia
* K sparing diuretics
* ACE inhibitors
* ARBs
* NSAIDs
* Bactrim
36
3 ways increased inake of K can cause Hyperkalemia
* Increased dietary intake of K containing foods
* Taking too much PO potassium
* Taking too much IV potassium
37
**Other causes of Hyperkalemia**
* 3 conditions which move K from intracellular to extracellular spaces
* Tissue damage (rhabdomyolysis)
* Acidosis
* Decreased insulin
38
2 emergent treatment options for tx of Hyperkalemia
* **IV Calcium**
* **Maneuvers to shift K from ECF to ICF**
* Sodium bicarbonate (IV push)
* Insulin IV + D50W (given w/ dextrose)
39
**Which emergent tx of Hyperkalemia?**
* Less than 5 mins onset of action
* Lasts 60 minutes
* Reduces threshold potential of cardiac myocytes, restoring the normal gradient with the resting membrane potential which is distorted by hyperkalemia
IV Calcium
40
**Which emergent tx of Hyperkalemia?**
* IV push to increase pH
* Action within 5 mins
* Lasts 15-30 mins
* Typically start with 1 amp = 50 mEq
Sodium Bicarbonate
| (shifts K from ECF to ICF)
41
Other potential options for emergent tx of Hyperkalemia (3)
* Nebulized albuterol
* IV Lasix
* Dialysis
42
**Which "less urgent" tx of Hyperkalemia?**
* Exchanges Na for K in the gut
* Decreases total body K
* Causes lots of horrible diarrhea
* Onset 2-12 hours, available PO or PR
* Lowers K level by 0.5 for every gram given
**What are 2 other less urgent tx options?**
Kayexalate
* Lasix (and other loop & thiazide diuretics)
* Correct underlying cause
43
Measure of total Ca is ___ + \_\_\_\_
Free (ionized) + protein bound
44
Serum calcium is used to evaluate metabolism and monitor patients w/ what 3 things?
* Hyperparathyroidism
* Malignancies
* Renal Failure
45
Calcium has an inverse relationship with what chemical compound?
Phosphate
46
* 99% of Ca is located where in the body?
* ECF Calcium
* 50% is \_\_\_\_
* 10% is \_\_\_\_\_
* 40% is \_\_\_\_
Bone
* 50% is free (ionized)
* 10% is complexed
* 40% is protein bound
47
**Which form of calcium?**
* Physiological active form, unaffected by serum albumin levels
* Free to participate in cellular function
* role in neuromuscular activity, cardiac function, and blood clotting
Ionized
48
**Which form of Calcium?**
* Citrate added to blood to prevent clotting
**Complexed** (chelated with substances such as citrate)
49
**Which form of Calcium?**
* When serum albumin is low, Ca level will also be low
* Albumin and Calcium should be measured silmultaneously
Protein - bound (albumin)
50
**Calcium Physiology**
* Calcium is absorbed through ____ under influence of \_\_\_\_\_
* Stored where?
* Excreted by what organ?
* Regulated by what 3 things?
* GI tract / Vitamin D
* Bone
* Kidney
* PTH / Vit D / Calcitonin
51
A decrease in serum Calcium triggers the release of ___ from the parathyroid gland, which acts to increase Ca in the blood by doing what 3 things?
PTH
* Activating Vit D (to increase Ca absorption in gut)
* Promoting bone resorption (release Ca from bone)
* Increasing Ca uptake in the kidneys (Promotes conservation)
52
An increase in serum Calcium triggers the release of ____ from the thyroid gland, which acts to decrease Ca in blood by doing what?
Calcitonin
* Inhibiting bone resorption
53
If calcium levels are high, what should you be concerned about?
Malignancy
54
Sxs of Hypercalcemia
"Has a cute saying to remember"
**"Stones, bones, abdominal moans, and psychiatric groans"**
* Kidney stones
* Bone pain
* Abd pain, N/V, anorexia, constipation
* Effects of nervous system, lethargy, fatigue, memory loss, psychosis, depression
55
What 2 things cause 90% of hypercalcemia?
* Malignancy
* Primary hyperparathyroidism
56
Which 4 medications can cause hypercalcemia?
* Thiazide diuretics
* Lithium
* Antacids
* Vitamin A analogs (accutane)
57
**Evaluation of Hypercalcemia**
* PTH is increased with \_\_\_\_\_
* PTH is suppressed in \_\_\_\_\_
* Increased in primary hyperparathyroidism
* Suppressed in malignancy
58
* What is the #1 therapy / tx of Hypercalcemia?
* What are 3 other tx options?
* _\*\*#1: Volume expansion (normal saline)_
* **Calcitonin** (used to lower levels rapidly)
* **Pamidronate** (usually given to cancer pts)
* **Zoledronic Acid** (Zometra - replaced Pamidronate as a 1st line therapy for malignancy)
SG F2 E5
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