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Adult 1 Exam 1 > 2. F&E 2 > Flashcards

2. F&E 2 Flashcards

1
Q

Hyponatremia causative factors:

A

Vomiting, diarrhea, fistulas, sweating
Diuretics, low salt diets, deficiency of aldosterone
Water intoxiction - causes water to move into the cell = ECF volume excess; seen with inappropriate ADH; hyperglycemia, tap-water enema; irrigation of g-tubes with water instead of NS; compulsive water drinker; excessive use of IV Dextrose and Water
-SIADH

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2
Q

SIADH

A

syndrome of inappropriate ADH, so increase AHD (reabsorbs water and sodium filling up urine)
Leads to inappropriate urination of sodium
Conditions associated w SIADH = oat-cell lunc tumors, head injury, endocrine and pulmonary disorders; physiologic and psychological stress; medications – chemo agents

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3
Q

Hyponatremia s/s

A

Headache, orthostatic BP, nausea, abdominal cramping, altered mental status, can have seizures that lead to coma, poor skin turgor, dry mucosa, decreased saliva production, Anorexia, muscle cramps, exhaustion; serum sodium below 115 mEq/L; signs of increased intracranial pressure – lethargy, confusion, muscle twitching, focal weakness, hemiparesis, seizures

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4
Q

Hyponatremia treatment

A

Sodium replacement – by mouth, nasogatric tube, or IV

Water restriction – total 800 ml / 24 hours

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5
Q

Hypernatremia patho

A

fluid deprivation in unconscious patients who cannot perceive, respond to, or communicate thirst; Very old, very young, cognitively impaired persons

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6
Q

Hypernatremia causative factors:

A

Fluid deprivation, hypertonic enteral feedings (Adminstration without water supplements); watery diarrhea, hyperventilation, burns, diabetes insipidus (polydispia – increase urination, holding on to salt)
Less common causes: heat stroke, near-drowning in sea water, malfunction of HD or PD systems, IVF – hypertonic saline

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7
Q

Hypernatremia s/s

A

Neurologic (primarily neurologic – consequence of cellular dehydration – concentrated ECF), diminished DTR, restlessness, weakness, disorientation, delusions, hallucinations; thirst, dry/sticky mucus membrane, red/dry tongue; body temp rises

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8
Q

Hypernatremia treatment

A

monitor how quick, want gradual change back to normal - Gradual lowering of serum sodium by infusion of hypotonic electrolyte solution – 0.3% sodium chloride) or an isotonic nonsaline solution (D%W) – as indicated when water needs to be replaced without sodium
may give diuretics for fluid overload - to treat sodium gain
may need dialysis
monitor fluid loss

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9
Q

Hypokalemia

A

o Indicates an actual deficit in total K+ stores

o GI loss most common cause; vomiting and gastric suction may lead to hyokalemia

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10
Q

Hypokalemia causative factors

A

Diuretics, vomiting, gastric suction, diarrhea, hypersecretion of insulin, dietary, debilitated, elderly, alcoholism, anorexia, bulimia

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11
Q

Hypokalemia s/s

A

Cardiac or respiratory arrest, dysrhythmia, digitalis sensitivity, flat/inverted T wave on EKG; alkalosis; fatigue, anorexia, N/V; muscle weakness, leg cramps, decreased bowel motility (muscle contractions), paresthesias
- symptoms not likely unless beow 3.0 mEq/L

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12
Q

Hypokalemia treatment

A

Dietary or IV intake – give potassium by mouth if able, if not then dilute and give by IV - Cannot give undiluted potassium, will kill pt
• Increased intake of dietary K+, or IVF therapy, 40-80mEq/day is adequate in adults
• Foods = fruit – raisins, banana, apricots, organes, vegetables, legumes, whole grains, milk, and meat, Salt substitutes contain 50-60 mEq of K+ per teaspoon

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13
Q

Hyperkalemia

A

Seldom occurs with normal renal function - is often due to treatments of other conditions
Cardiac arrest more common with elevated K+
Causes of “pseudo” hyperK+ : tight tourniquet around exercising extremity while drawing a blood sample and hemodialysis of sample before analysis
eukocytosis (WBC > 200,000); thrombocytosis (platelets > 1 million); drawing blood above K+ infusion site Measurements should be verified

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14
Q

Hyperkalemia causative factors

A

Renal failure; deficient adrenal hormones; medications; diet; burns, tissue trauma, may be because of shortening of dialysis

  • Major cause: decreased renal excretion of K+ - untreated renal failure; hypoaldosteronism and Addison’s disease (deficient adrenal hormones)
  • Medications – KCL, heparin, angiotensin-converting enzyme inhibitors, captopril, nonsteroidal antiinflammatories, K= sparing diuretics
  • High dietary intake; K+ supplements; IVF;
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15
Q

Hyperkalemia s/s

A
  • Peaked T waves, widen QRS on EKG; cardiac arrest; acidosis
  • Skeletal muscle weakness; numbness, paresthesia, paralysis
  • Nausea, colic, diarrhea, abdominal cramping
  • cardiac effects not usually significant below 7 mEq/L but almost always present when 8 mEq/L or greater
  • Earliest changes – narrow T wave, ST segment depression, shortened QT interval (6 mEq/L) if levels continue to increase, PR interval prolonged – disappearance of P wave; ventricular dysrhythmias, cardiac arrest
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16
Q

Hyperkalemia treatment

A
  • Restrict K+ intake – oral and IV, eliminate salt substitutes
  • Retention enema; Kayexalate – orally or retention enema (do not use if paralytic ileus or intestinal perforation can occur)
  • EKG to detect changes; repeat serum K+ level from vein
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17
Q

Hypocalcemia causative factors

A

Hypoparathyroidism, also associate with surgery on thyroid and parathyroid glands and radical neck dissections, Inflammation of pancreas; renal failure; insufficient Vitamin D; Magnesium deficiency; thyroid carcinoma; low albumin, alkalosis, alcohol abuse

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18
Q

Hypocalcemia s/s

A

Tetany, tingling fingers, mouth, feet; spasms in extremities or face; seizures; mental changes, delirium; prolonged QT interval on EKG, Ventricular tachycardia

  • tetany – the entire symptom complex induced by increase neural excitabilty – sx due to spontaneous discharges of both sensory and motor fibers in peripheral nerves
  • Trousseau’s sign – inflate bp cuff, carpal spasms (abduction thumb, flexed wrist, fingers together)
  • Chvosterk’s sign - tap side of cheek and notice twitching
  • seizures may occur – increased irritability of CNS; mental changes – depression, impaired memory, confusion, delirium, hallucination
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19
Q

Hypocalcemia assessment

A

Serum calcium, albumin Level, arterial pH; PTH level; Magnesium & phosphorus levels

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20
Q

Hypocalcemia treatment

A

Calcium salts via IVF therapy; Vitamin D therapy; aluminum hydroxide antacids; dietary replacement

  • acute symptoms are life-threatening and require prompt treatment with IV calcium
  • Parenteral calcium salts – calcium gluconate, calcium chloride, calcium gluceptate
  • Too rapid IV admin can cause cardiac arrest – dangerous in patients receiving digitalis-derived meds
  • IV calcium should be diluted in D5W –given slow IV bolus or slow IV infusion (0.9% NS should NOT be used with calcium because it increases renal calcium loss)
  • Solutions with phosphates or bicarb should NOT be used -> percipitates when calcium is added
  • Calcium can cause postural hypotension – keep in bed for IV replacement and monitor BP
  • Vit D therapy – increase calcium absorption from GI tract
  • Aluminum-hydroxide antacids
  • Dietary intake to at least 1000 – 1500 mg/day in adult
  • Foods high in calcium = milk products, green leafy vegetable, canned salmon, sardines, fresh oysters
21
Q

hypercalcemia crisis

A

17** severe thirst and polyuria; muscle weakness, intractable nausea, abdominal cramps, obstipation or diarrhea, peptic ulcer symptoms, bone pain; lethargy, confusion, and coma – very dangerous condition – may lead to cardiac arrest.
• mortality rate as high as 50% if not treated promptly.

22
Q

hypercalcemia causative factors

A

Malignancy, bone cancer, hyperparathyroidsim ; excessive PTH (secretion = increased release of calcium from bones and increased intestinal and renal absorption); immobilization (Bone mineral is lost during immobilization – may cause increase in total calcium); thiazide diuretics (may cause slight elevation – they potentiate the action of PTH on kidneys = reduced urinary calcium excretion); vitamin A & D intoxication, lithium

23
Q

hypercalcemia s/s

A

Muscle weakness, depressed DTR, uncoordination; lethargy, confusion, coma, short QT on EKG; renal stones

  • hyper ca+ reduces neuromuscular excitability – suppresses activity at myoneural junction
  • Muscle weakness, incoordination, anorexia, constipation
  • Cardiac standstill may occur when serum calcium is 18mg/dl
  • Dig toxicity is aggravated by hypercalcemia
  • Anorexia, N/V, constipation; dehydration; abdominal / bone pain; abdominal distention and paralytic ileus; excessive urination; severe thirst; peptic ulcer sx – increased secretion of acid and pepsin by stomach
  • Confusion, impaired memory, slurred speech, lethargy, acute psychotic behavior, or coma may occur
24
Q

hypercalcemia treatment

A

Treat underlying cause; IVF therapy; mobilize patient; restrict dietary intake

25
Q

Hypomagnesemia

A

o Approximately 1/3 of Mg is bound to protein the rest is free cations
o Should be evaluated with albumin levels – low albumin levels will decrease total Mg
o Route for loss: GI tract – NG suction, diarrhea, fistulas
o Mg concentration is higher in lower GI tract so diarrhea and fistuala will cause greater deficit
o The distal small bowel is where most Mg is absorbed so any disruption (intestinal resection, inflammatory bowel disease) can lead to hypoMg

26
Q

Hypomagnesemia causative factors

A
  • Alcohol withdrawal - Withdrawal from alcohol is most common cause in US (should be measured q 2-3 days)
  • Malnutrition, malabsorption - Administration of nourishment – TPN or tube feedings
  • Other causes: aminoglycosides, cyclosporine, diuretics, digitalis, amphotericin, and citrated blood – especially in pt with renal or hepatic disease
  • Diabetic ketoacidosis – secondary to increased renal excretion duiring osmotic diuresis – Mg shifts into the cells with insulin therapy
  • Contributing causes: sepsis, burns, and hypothermia
27
Q

Hypomagnesemia s/s

A

Hyperexcitability with muscle weakness, tremors; tetany, seizures; mood alterations; cardiac dysrhythmias

  • sx usually not seen until level <1 mEq/L
  • neuromuscular – hyperexcitability w/ muscle weakness, tremors, athetoid movements (slow, involuntary twisting and writhing)
  • Tetany, generalized tonic-clonic or focal seizures, laryngeal stridor,
  • ECK – prolonged QRS, depress ST segment, and predisposed to cardiac dysrhythmias – PVC, supraventricular tachycardia, V-fib
  • Increased susceptibility to digitalis toxicity
  • May also see marked alterations in mood – apathy, depression, apprehension, or extreme agitation
  • Ataxia, dizziness, insomnia, confusion, delirium, auditory/visual hallucinations, psychoses
28
Q

Hypomagnesemia treatment

A

Dietary; IVF therapy; monitor urine output

29
Q

Hypermagnesemia

A

May be falsely elevated when blood hemolyze or is drawn from extremity with excessively tight tourniquet

30
Q

Hypermagnesemia causative factors

A

Renal failure; untreated diabetic ketoacidosis; excessive administration of Magnesium; excessive use of antacids and laxatives

  • Most common cause: renal failure
  • May occur in patient with untreated diabetic ketoacidosis when catabolism causes the release of cellular Mg that cannot be excreted because of profound fluid volume depletion and oliguria.
  • Excessive administration to treat eclampsia or to lower serum Mg levels
  • Adrenocortical insufficiency; Addison’s disease, hypothermia; excessive use of antacids (maalox, Riopan) and laxatives (MOM)
31
Q

Hypermagnesemia s/s

A

Low BP, N/V, soft-tissue calcification; facial flushing; sensation of warmth;

  • High levels = lethargy; dysarthria; drowsiness; DTR lost; muscle weakness/paralysis may occur; cardiac & respiratory arrest if untreated
  • depressed CNS and peripheral neuromuscular junction
  • Tendency to low BP due to peripheral vasodilation;
  • N/V, soft-tissue calcification; facial flushing, sensation of warmth;
  • High levels = lethargy, difficulty speaking, drowsiness; deep tendon reflex may be lost; muscle weakness and paralysis may develop
  • Resp center is depress when serum Mg exceed 10 mEq/L – coma, atrioventricular heart block and cardiac arrest may occur if left untreated
32
Q

Hypermagnesemia treatment

A

EKG monitor; ventilate if necessary; hemodialysis; IVF therapy

  • Avoid administration of Mg with renal failure;
  • Carefully monitor those receiving Mg salts – D/C use if hyperMg
  • Emergencies – Resp. depression or defective cardiac conduction – may require venilatory support and IV calcium
  • Hemodialysis with Mg-free dialysate can reduce Mg to safe level within hours
  • Loop diuretics and 0.45%NS enhance Mg excretion if adequate renal function
  • IV calcium gluconate antagonizes the neuromuscular effects of Mg
33
Q

Hypophosphatemia

A

(phosphorus and calcium have an inverse relationship)
Although it often indicates phosphorus deficiency – it may occur under a variety of circumstances - May be hypo – even if normal body stores are normal –
Phosphorus deficiency is an abnormally low content of phosphorus in lean tissues and may exist in the absence of hypophosphatemia

34
Q

Hypophosphatemia causative factors

A

Malnutrition; alcohol withdrawal; elderly; debilitated; diabetic ketoacidosis; burns; certain antacids;Vitamin D deficiency

  • Often seen during administration of calories to patient with severe protein-calorie malnutrition
  • Likely to occur with overzealous intake or administration of simple carbohydrates
  • Examples: anorexia, alcoholism, elderly, debilitated, those unable to eat
  • As many as 50% alcoholics will have hypoPh
  • May be seen in malnourished pt receiving TPN
  • Prolonged hyperventilation, alcohol withdrawal, poor dietary intake, diabetic ketoacidosis, major thermal burns
  • Resp. alkalosis
  • Excess-phosphorus binding by antacids containing Mg, calcium or albumin may decrese phosphorus available from the diet to amount below that required to maintain serum balance
  • Vitamin D regulates intestinal absorption – deficiency of Vit D may cause decreased calcium and phosphorus levels = osteomalacia (softened, brittle bones)
35
Q

Hypophosphatemia s/s

A

Irritability, weakness, numbness, confusion, seizures, coma; hypoxia, bruising or bleeding

  • irritability, fatigue, apprehension, weakness, numbness, paresthesias, confusion, seizures, coma
  • Hypoxia -> increased resp rate & alkalosis
  • hypoPh predisposes a person to infection
  • Muscle weakness, muscle pain; weakness of respiratory muscles may impair ventilation
  • HypoPh may predispose to insulin resistance and hyperglycemia
  • Chronic loss of phosphorus can cause bruising and bleeding from platelet dysfunction
36
Q

Hypophosphatemia treatment

A

IVF therapy; monitor concentration of enteral feedings; oral supplements; monitor serum phosphate

37
Q

Hyperphosphatemia causative factors

A

Renal failure; hypoparathyroidism; diabetic ketoacidosis; diet intake

  • Various conditions can lead to this imbalance – renal failure is most common
  • Others: chemotherapy for neoplastic disease, hypoparathyroidism; resp acidosis or diabetic ketoacidosis, high phosphate intake, profound muscle necrosis, increase phsophorus absorption
38
Q

Hyperphosphatemia s/s

A

Related to decreased calcium= tetany; anorexia, N/V; muscle weakness; hyperreflexia; tachycardia; soft tissue calcification

  • Most result from decreased calcium level and soft tissue calcifaction
  • Tetany – causing tingling sensation in fingertips and around mouth
  • Anorexia, N/V, muscle weakness, hyper-reflexia; tachycardia
  • Long-term consequence: soft-tissue calcification – seen with reduced glomerular filtration rates
  • High levels promote precipitation of calcium phosphate in nonosseous sites, decreasing urine output, impairing vision, and producing palpitations
39
Q

Hyperphosphatemia assessment

A
  • Serum phosphate level over 4.5 (normally higher in children because of high rate of skeletal growth)
  • Serum calcium useful for diagnosing primary problem and assessing effect of treatments
  • X-ray to show skeletal changes
40
Q

Hyperphosphatemia treatment

A

Treat underlying cause (renal or parathyroid) IE: renal failure – measure to decrease serum phosphate are indicated – administer phosphate-binding gels, restrict dietary intake and dialysis

41
Q

Hypochloremia causative factors

A

Deficient intake or reabsorption; salt-restricted diets; GI tube drainage; severe vomiting or diarrhea, worry about GI suctioning

  • Chloride control depends on intake of chloride and excretion and reabsorption of its ions in the kidneys
  • Chloride produced in stomach as hydrochloric acid – small amount is lost in feces
  • Risk factors = salt-restricted diets, GI tube drainage, severe vomiting & diarrhea
42
Q

Hypochloremia s/s

A

Same as with sodium & potassium deficit and metabolic alkalosis; hyperexcitability of muscle; tetany; hyperactive DTR; weakness, twitching; cramps; cardiac dysrhythmia; seizures

  • acid-base and el+ imbalances
  • Hyponatremia, hypokalemia, and metabolic alkalosis (high pH and high bicarb)
  • Hyperexcitability of muscles, tetany, hyperactive DTR, weakness, twitching, muscle cramps
  • Cardiac dysrhythmia and seizures as noted with other El+ changes
43
Q

Hypochloremia assessment

A

Serum chloride ; Sodium and K+ levels; ABG; Urine chloride

44
Q

Hypochloremia treatment

A

IVF therapy; D/C or change diuretics; dietary intake; ammonium chloride;

  • Correct the cause –
  • IVF therapy with 0.9% or 0.45% NS is used
  • May D/C use of diuretics or change to another kind
  • Foods high in chloride = tomato juice, salty broth, canned vegetables, processed meats, and fruits
  • Avoid large amounts of free / bottled water because it causes body to excrete large amounts of chloride
  • Ammonium chloride – an acidifying agent may be Rx for metabolic alkalosis
  • Monitor I & O, ABGs, vital signs, respiratory status
45
Q

Hyperchloremia causative factors

A

Loss of bicarbonate ions via kidney or GI tract with corresponding increase in chloride ions

46
Q

Hypochloremia s/s

A

Same as with hypernatremia; metabolic acidosis; tachypnea; weakness; lethargy; deep rapid resp; diminished cognitive ability; hypertension

  • same as metabolic acidosis; hypervolemia; hypernatremia
  • Tachypnea; weakness; lethargy; deep, rapid resp; diminished cognitive ability; hypertension
  • If untreated – decrease in cardiac output; dysrhythmia; coma
  • High Chloride is seen with high sodium and fluid retention
47
Q

Hypochloremia assessment

A

Serum chloride 108 or greater; Sodium > 145; pH < 7.35, Bicarb < 22, Normal anion gap, Urine excretion increases

48
Q

Hypochloremia treatment

A

IVF Therapy with LR; diuretics, restrict sodium and chloride; monitor vital signs, I & O

  • Correct cause – restore El+, fluid, an acid-base balance
  • Lactated Ringer’s may be used to convert lactate to bicarb in liver - > increase base bacarb level and correct acidosis
  • Sodium bicarb may be given IV to promote renal excretion
  • Diuretics may be used to eliminate chloride
  • Restrict sodium, fluids, and chlorides
  • Monitor vital signs, ABG, I & O
  • Respiratory, neurologic and cardiac systems

Adult 1 Exam 1 (15 decks)

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