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Week 4
Potassium, Calcium & Magnesium Homeostasis and Imbalances
| Question | Answer |
|---|---|
| What is an ion? | Charged molecule |
| What is the chemical symbol for potassium? | K+ |
| What is the chemical symbol for calcium? | Ca++ |
| What is the chemical symbol for magnesium? | Mg++ |
| What are the principles of electrolyte homeostasis and imbalances? (4) | 1. Intake and absorption 2. Distribution 3. Excretion 4. Loss through abnormal routes |
| To maintain homeostasis, ___ + ____ must equal ____ + ____ | Intake, absorption; excretion, loss |
| Which electrolyte imbalances are “floppy”? | Hyperkalemia, hypokalemia, hypercalce,ia, hypermagnesemia |
| Which electrolyte imbalances are “twitchy”? | Hypocalcemia, hypomagnesemia |
| Potassium ions are necessary for normal function of all cells, especially ___ and ____ cells | Neurons, muscle cells |
| The ratio of potassium inside/outside of the cell determines its ____ potential. | RMP: resting membrane potential |
| Most of the potassium ions in the body are _____ the cells | Inside |
| The sodium-potassium pump used ____ to maintain cell homeostasis | ATP |
| Normal muscle cells have a very small electrical charge across their membranes, called the ______. | Resting membrane potential |
| If potassium ratio is altered, _______ will be different and muscle can have abnormal function. | Resting membrane potential |
| Potassium imbalances can affect... | Function of skeletal muscle, smooth muscle and/or heart muscle |
| The word ‘potassium’ comes from the word ____ | Potash, meaning plant residue |
| How do we take in potassium? | Through diet, or potassium-containing medication |
| What foods contain potassium? | Fruits- bananas, oranges, raisins, cantaloupe, apricots. Vegetables- Asparagus, bok choy, broccoli, carrots, celery. Other- nuts, molasses, sunflower seeds |
| What mechanism pumps K+ ions into cell to keep intracellular K+ level high? | Sodium-potassium pump |
| What causes K+ to move from plasma into cells? | Alkalosis, insulin, and beta-adrenergic stimulation |
| What causes K+ to move from cells into plasma? | Acidosis due to mineral acids (caused by bicarbonate loss in diarrhea) |
| Potassium is normally excreted in... | Urine, feces, sweat |
| More potassium is excreted than normal in ____ | Diarrhea |
| Potassium excretion by the kidneys is ____ dependent | Flow dependent |
| Flow-dependent excretion of K+ in kidneys means... | The larger the urine volume, the more potassium is excreted |
| What hormones increase potassium excretion in the urine? | Aldosterone, glucocorticoid hormones (cortisol) Aldosterone pulls in ___ from the urine, and pushes ___ out |
| Potassium may be lost through abnormal routes via.... | emesis, drainage from tubes inserted into the GI tract (nasogastric tubes), or other losses of body fluids |
| What is hypokalemia? | Serum potassium concentration that is below normal (< 3.5 mEq/L). Plasma deficit of K+, whole body K+ may be decreased, normal, or increased |
| With hypokalemia, whole body potassium levels may be... | Decreased, normal or increased |
| What are the 4 general risk factors for hypokalemia? | 1. Decreased K+ intake 2. Shift of K+ from plasma into cells 3. Increased K+ secretion 4. Loss of K+ through abnormal route |
| What are risk factors for decreased potassium intake? | Anorexia; unusual weigh-loss diets that do not contain K+; NPO orders; prolonged IV therapy without K+ |
| What are risk factors that shift K+ from plasma into cells? | Alkalosis; hypersecretion of insulin (response to TPN- total parenteral nutrition); insulin overdose; excessive beta-adrenergic stimulation (epinephrine, albuterol); hypothermia |
| What does insulin do to K+ in the plasma? | Moves K+ into cells |
| What are risk factors for increased K+ excretion? | medications that cause increased K+ excretion in urine); increased effect of aldosterone (hyperaldosteronism, CHF, cirrhosis); hypomagnesemia; black licorice; diarrhea, laxative overuse, colon cleansing/irrigation |
| What causes loss of K+ through abnormal routes? | Emesis, nasogastric suction, intestinal decompression |
| What are some clinical signs of hypokalemia? | Abdominal distention, decreased bowel sounds, constipation, paralytic ileus (GI not moving); polyuria; orthostatic hypotension; flaccid skeletal muscle weakness; flaccid paralysis; cardiac dysrhythmias; quadriceps weakness |
| Cardiac dysrhythmias can be caused by | Both hypokalemia and hyperkalemia |
| Quadricep weakness is a sign of ____ | Hypokalemia |
| Why is hypokalemia a “floppy” disorder? | Hyperpolarization makes it harder to reach action potential (more negative) |
| What are important teachings for a patient with hypokalemia? | Safe weight loss diet, bowel management to prevent diarrhea from laxative overuse. need for increased K+ intake to offset loss in diarrhea; K+ rich foods |
| What is hyperkalemia? | Serum potassium concentration that is above normal (>5.0 mEq/L). Indicates a plsma excess of K+ |
| In hyperkalemia , the whole body K+ level may be... | Increased, normal or decreaed |
| What are the 3 general risk factors fro hyperkalemia? | Increased K+ intake, shift of K+ from cells to plasma, decreased K+ excretion |
| What are risk factors for increased K+ intake? | Oral intake is rarely a problem unless combined with decreased urine output. Too much/rapid KCl; insufficient mixing of KCl in IV bag; stored blood (K+ leaks out of cells into plasma in old blood); large does of penicillin G |
| When is use of stored blood an issue? | When using large amounts ≥ 8 unitsl blood older than 3 days |
| What risk factors shift K+ from cells into plasma? | Acidosis due to mineral acids (loss of bicarbonate in diarrhea); crushing injury or massive cell death; insulin deficiency |
| What risk factors cause decreased K+ excretion? | Mediations, oliguric renal disease, severe hypovolemia , decreased aldosterone effect |
| How does severe hypovolemia cause decreased K+ excretion? | Decreased ECV causes decreased kidney perfusion, producing less urine and excreting less K+ |
| What are some clinical signs of hyperkalemia? | Intestinal cramping and diarrhea; flaccid skeletal muscle weakness; flaccid paralysis; cardiac dysrhythmias |
| Which electrolyte imbalance causes most potentially dangerous dysrhythmias? | Hyperkalemia |
| What are some important teachings for patients with hyperkalemia? | Stop K+ containing preparations (KCl based salt substitutes), if urine volume decreases; reduce intake of K+ rich foods) |
| What normal ranges for serum calcium? | 9-11 mg%; 4.5-5.5 mEq/L |
| Lab reports measure ____ calcium | Total calcium |
| True or false: ionized calcium can be measured with low/high total calcium. | True |
| What is the physiologically active form of calcium? | Free, ionized calcium |
| Are calcium ions bound to albumin physiologically active? | No. Physiologically inactive while bound |
| Are calcium ions bound to small organic anions like citrate physiologically active? | No. |
| Plasma calcium and plasma ____ vary inversely | Plasma phosphate |
| What decreases the amount of physiologically available Ca++? | Alkalosis. Bicarbonate binds to Ca++ |
| Which hormone regulates plasma Ca++ concentration? | Parathyroid hormone (PTH) |
| What does PTH do? | Increases plasma Ca++: takes it from bones and improves absorption of vitamin D needed for Ca++ absorption. |
| Where is calcium absorbed? | Duodenum (more acidic) |
| What is hypocalcemia? | Plasma deficit of Ca++l serum levels may not reflect body stores |
| What are the 4 general risk factors for hypocalcemia? | Decreases Ca++ intake or absorption; decreased physiological availability of Ca++; Increased Ca++ excretion; loss of Ca++ by abnormal route |
| What risk factors cause decreased Ca++ intake or absorption? | Chronic malnutrition or poor calcium intake, vitamin D deficiency (lack of sunlight); antacid overuse (non-calcium); chronic diarrhea (includes laxative overuse); steatorrhea |
| Why does antacid overuse cause decreased calcium absorption? | Because the bicarbonate in antacids makes GI less acidic |
| What is steatorrhea? | Floating fats in stools (such as in pancreatitis) bind and excrete Ca++ |
| What risk factors cause decreased physiological availability of Ca++? | Massive transfusion with citrated blood; hypoparathyroidism (that includes removal of parathyroid glands); alkalosis (decreased acidity); overuse of phosphate-containing laxatives and enemas |
| What are clinical signs of hypocalcemia? | Positive Chvostek sign, positive Trousseau sign; muscle twitching, cramping; carpopedal spasm, tetany; laryngospasm; seizures, cardiac dysrhythmias |
| Why is hypocalcemia a twtitchy disorder? | Depolarization makes it easier to reach action potential |
| What are important teachings patients with hypocalcemia? | Bowel management to prevent laxative overuse; calcium rich foods; alternate Ca++ sources for those who do not eat dairy; need or increased Ca++ for those with chronic diarrhea or malabsorption |
| What are some calcium rich foods? | Milk, dairy products; almonds, cream of wheat and farina cereal; chocolate, canned fish (with bones); oranges; oysters, tofu, dark leafy greens, corn tortillas |
| What is hypercalcemia? | excessive plasma Ca++ |
| What are some general risk factors of hypercalcemia? | Increased Ca++ intake/absorption; shift of Ca++ from bones to plasma; decreased Ca++ excretion |
| What risk factors cause shift of Ca++ from bones to plasma? | prolonged immobilization, cancers, bone tumors, hyperparathyroidism, ectopic release of parathyroid- hormone related peptide |
| Is hypercalcemia floppy or twitchy ? | floppy |
| What are some clinical signs of hypercalcemia? | Anorexia, constipation, nausea and emesis, muscle weakness, fatigue, confusion and lethargy, personality and mood changes; polyuria |
| What are important teachings for a patient with hypercalcemia? | Avoid massive vitamin D supplementation; need for adequate hydration to prevent renal damage with hypercalcemia |
| What are normal ranges for serum magnesium? | 1.5-2.5 mEq/L |
| What are parts of total body magnesium? | Ionized magnesium (physiologically active form), Mg++ bound to albumin (physiologically inactive); Mg++ bound to small organic anions like citrate (physiologically inactive) |
| Magnesium is absorbed primarily from the ____ | Terminal ileum |
| What is hypomagnesemia? | Plasma Mg++ deficit |
| More Mg++ mean less ____ | Ach |
| Hypomagnesemia means less magnesium, more Ach released from motor nerve | Twitchy |
| What are the general risk factors for hypomagnesemia? | Decreased Mg++ intake or absorption; decreased physiologically availability of Mg++; increased Mg++ excretion; loss of Mg++ by abnormal route |
| What risk factors cause decreased Mg++ intake? | Malabsorption syndromes, chronic diarrhea, steatorrhea, chronic malnutrition, chronic alcoholism, ileal resection |
| What risk factors cause increased Mg++ excretion? | Diuretic therapy, diabetic ketoacidosis, hyperaldosteronism, chronic alcoholism, steatorrhea |
| What risk factors cause loss of Mg++ through abnormal route? | Acute pancreatitis |
| What are some clinical signs of hypomagnesemia? | Insomnia, hyperreflexia, positive Chvostek sign, positive Trousseau sign, skeletal muscle cramps, twitching, tremors, tetany, nystagmus, seizures, extreme confusion, cardiac dysrhythmias |
| Is hypomagnesemia floppy or twitchy? | Twitchy. Less Mg++ mean MORE ACH |
| What are important teachings for a patient with hypomagnesemia? | Information about alcoholism treatment, if applicable. Mg++ rich foods |
| What foods are rich in Mg++ | Dark chocolate, nuts, dark green vegetables, legumes |
| What is hypermagnesemia? | Plasma Mg++ excess |
| What are the general risk factors for hypermagnesemia? | Increased Mg++ absorption, decreased Mg++ excretion |
| What risk factors cause increased Mg++ absorption? | Excessive use of Mg++ (antacids) |
| What risk factors cause decreased Mg++ excretion? | oliguric renal disease, adrenal insufficiency |
| What are some clinical signs of hypermagnesemia? | Hypotension, drowsiness, lethargy, weak or absent deep tendon reflexes, flaccid muscle paralysis, respiratory depression, cardiac dysrhythmias |
| What are some important teachings for a patient who has hypermagnesemia? | Replace chronic Mg++ laxative use with alternative methods of bowel management for older adults; avoid Mg++ containing antacids and laxatives if urine volume decreases |
| Which electrolyte imbalances cause cardiac dysrhythmias? | All except hypercalcemia |
Created by:
kangaloo
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