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Hyper/o Na+ K+

Clinical Medicine II

What is most common cause of hypernatremia not enough water intake
Three types of hypernatremias Hypovolemic, euvolemic, hypervolumic
In the hospital, what is the MC cause of hypernatremia Hypervolemia and hypernatremia d/t IVs
Why do pregnant women hyperventilate to keep babies CO2 nl, we need to ↓ our CO2.
Causes for hypervolumic, hypernatremia saline administration, sodium bicarb, primary hyperaldosteronism
What are the two defense mechanisms against hypernatremia stimulation of ADH (results in max [urine]), and thirst
What diminishes thirst ACEi and age
What causes orthostatic hypotension ↓ intravascular volume
When we are trying to ↑ BP what do we give NS, ~75% stays in intravascular volume
What is edema proportionate to the level of Na+ (edema? Nl BP? Give D5W)
When is hypernatremia more common after age 60 d/t ↓ thirst etc
What two hormones come from post pit. oxytocin and ADH
What does urine concentration depend on hypertonic medullary interstitium, osmotic equilibrium of urine
What is the cause for central diabetes insipidus secretion of ADH is impaired through disruption of hypothalamic nuclei, (osmoreceptors)
Causes for CDI head trauma, hypoxic, or ischemic encephalopathy, idiopathic
Mechanism of nephrogenic DI inability for the kidney to respond to ADH
Causes of NDI lithium, osmotic diuresis, sickle cell anemia
S/S of NDI lethargy, weakness, irritability, hypereflexia, sz, coma, death
Simple symptoms of NDI polydipsia, polyuria, nocturia
Nl Na+ levels 135-145
Serum osmolarity of hypernatremic 290 mOsm/kg
Part of dx of DI urine osmolality of 200mOsm/kg
Tx hypernatremia drink water, lower the serum Na+ concentration by about 0.5 mEq/L/hr next 24 hrs
Why should rapid correction be avoided brain’s adaptive response to hypernatremia, and the potential risk of cerebral edema
If BP low and Na+ tx give water (saline, NS)
Why do give interosseous so water depleted, can’t find a vein
Tx for pt’s w/ euvolemic and hypernatremia water replacement alone (free water orally or 5% dextrose)
Tx for hypervol/Na+ remove salt excess source, administer diuretics, replace water
What measurement of Na+ will cause comas and szs <120mEq/L
s/s hyponatremia anorexia, nausea, lethargy, apathy Advanced: disorientation, agitation, szs, depressed reflexes, focal neuro deficits
causes of hyponatremia vomiting, diarrhea, excessive sweating, hypotonic fluid ingestion, recent surgery, psychiatric illness, CHF, cirrhosis, nephrotic syndrome (renal failure)
PE for hyponatremia ortho vitals, skin turgor, JVD, edema, wedge pressure
Causes of hypovolemic hyponatrmia renal loss: diuretics, etc, GI loss, skin loss, peritonitis
Causes of euvolemic hyponatremia ADH excess, pain, postop state, cortisol def, hypothyroidism, ↓ solute intake, psychogenic polydipsia
Causes of hypervolemic hyponatremia CHF, cirrhosis, nephrotic syndrome, acute and chronic renal failure
What is central pontine myelinolysis demyelination of the pons
What causes CPM rapid correction of hyponatremia
How can CPM occur raising serum Na + more than 25mEq/l or above-nl level in first 48 hrs
When is rapid correction ok if serious situation (only correct to 120), and if it was rapidly depleted then its ok
Tx of hyponatremia eliminate the cause, restrict water inake, NS, can correct to 120 fairly rapidly, then slow down
If K+ is low think what? iatrogenic
How is K+ maintained (1) aldosterone, (2) high sodium delivery to the collecting duct (eg, diuretics), (3) high urine flow (eg, osmotic diuresis), (4) high serum potassium level, and (5) delivery of negatively charged ions to the collecting duct (eg, bicarbonate
What is excretion ↑ by by (1) absence or relative deficiency of aldosterone, (2) low sodium delivery to the collecting duct, (3) low urine flow, (4) low serum potassium level, and (5) renal failure.
How is K+ maintained predominantly through the regulation of renal excretion. The most important site of regulation is the collecting duct, where aldosterone receptors are present.
How does insulin and glucagon affect K+ Insuline induces to go into cells, glucagon blocks entry
Three ways to ↓ serum K+ Insulin, Beta-andrenergic antagonists, pH alkalosis
What ↑ serum K+ An acute increase in osmolality causes potassium to exit from cells. An acute cell/tissue breakdown releases potassium into extracellular space.
Three ways that K↓ ↓ intake, shift from extracellular to intracellular, increased secretion
Best way to give someone K+ PO by their gut, b/c very good at absorbing (~90%) secreted as body K+ ↑
SE’s for K+ N/V/D
How can we give such large doses PO absorption is slower, insulin helps push K+ into cell
What can we give to our pt’s to help push K+ into cells BB’s (B-adrenergic drugs) (could also be a cause)
3 causes of hypokalemia dietary defiecnecy (tea and toast), ↑ excretion (MC), d/t diuretics, hyperaldosteronism, ↑ urine flow, vomiting 3)extracellular to intracellular space
Causes of mortality w/ hyperkalemia cardiac arrhythmias and death
S/S hypokalemia weakness and fatigue, dyspnea, constipations, abd distention, exercise intolerance
HTN w/ kypokalemia sugguest primary aldosteronisms, renal a. stenosis, licorice ingestion
Reasons for increased excretion of K+ ↑ excretion, endogenous mineralcorticosteroid excess, hyperaldosteroneism, adrenocorticoal carcinoma,
Why does aldosterone cause hypokalemia induces Na+ retention and K+ excretion
Barterr syndrome autosomal
Gitelman syndrome autosomal-recessive, hypokalemic metabolic alkalosis and ↓ BP compared to barter, it is milder
What drugs can induce hypokalemia diruetics, penicillins, bicarb, amphotericin B, gentamicin, isplatin, B-agonist intoxication
What does low serum bicarb suggest diarreah, tubular acidosis, carbonic anhydrase inhibitors
Tx hypokalemia ↓ K+ losses, replenish K+ stores, evaluate for toxicities, determine cause for future episodes
MC drug cause of hypokalemia diuretics
Nl K+ level 3.5-4.5
What is the dangerous level for hyperkalemia >5.5
EKG changes associated with hyperkalemia Peaked t waves, little to no P waves
What does the rhythm sometimes look like “sine” wave, V tach
Where is the most important role of regulation of K+ distal nephron, distal CT,
What is excretion is decreased by absence of aldosterone, ↓ Na+ deliverty to DT, ↓ urine flow, ↓ potassium, renal failure
Major intracellular cation K+
Nl GFR >90
With the kidneys, what disrupts K+ homeostasis GFR <10 (get ready for dialysis <20)
Fxns of K+ in body muscle contraction, regulation of heart contractility, important for kidney fxn
Daily requirements for K+ 1-1.4mmol/kg
Dietary sources for K+ dried fruits, legumes, meats, poultry, soy, bananas, beans
Causes of K+ excess ↑ intake, ↓ excretion, acidosis (shift from intracellular to extracellular space)
MC cause of K+ excess ↓ excretion d/t meds, DM, Sickle cell, renal failure, NSAIDS (prostaglandin inhibition)
Causes of K+ from intracellular to extracellular space hyperosmolait, rhabdomyolysis, tumor lysis, succinylcholine administration, insulin def, acute acidosis
Sxs excess K+ weakness/fatigue (MC), frank muscle paralysis, SOB, palpitations
Tx for K+ CRUCIAL Insulin and glucose- 10 units of regular insulin, any short acting + glucose, Beta agonist (albuterol), bicarb, kayexalate, dialysis
What is NOT a tx for ACUTE hyperkalemia kayexalate
Order for emergency hyperkalemia tx Ca++, bicarb, insulin, glucose, albuterol neb, dialysis
Created by: becker15
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