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Hyper/o Na+ K+
Clinical Medicine II
| Question | Answer |
|---|---|
| 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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