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MOD 3 > fluid and electrolyte disorders 2 > Flashcards

fluid and electrolyte disorders 2 Flashcards

1
Q

____ is one of the most abundant cations in the body where majority is found in the ICF

A

potassium

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2
Q

_____ is generally impermeable to potassium

A

cell membrane

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3
Q

potassium that leaves the cell is transported back inside by ____

A

Na/K/ATPase pump

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4
Q

Potassium plays a key roll in what 2 main things?

A
  1. muscle cell excitability
  2. nerve impulses
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5
Q

Potassium helps with ____ by being exchanged for H+ ions by kidneys

A

acid-base balance

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6
Q

what 3 substances all cause movement from ECF to ICF

A
  1. insulin
  2. catecholamines
  3. B-agonist
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7
Q

4 factors that promote lower serum potassium levels

A
  1. aldosterone
  2. insulin
  3. B-agonist activity
  4. alkalosis
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8
Q

4 factors that promote higher serum potassium levels

A
  1. cell lysis
  2. strenuous exercise
  3. a-agonist
  4. acidosis
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9
Q

potassium is regulated by activities of ion pumps, mostly distributed in the kidney:

A
  1. distal portions of nephron tubules and collecting system
  2. Na+ from tubular fluid is exchanged for either H+ or K+ in peritubular fluid
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10
Q

3 factors responsible for urinary excretion of potassium

A
  1. changes in conc of ECF
    - HIGH ECF conc INCREASES rate of secretion
  2. changes in pH
    - LOW ECF pH LOWERS peritubular fluid pH
    - H+ rather than K+ is exchanged for Na+ in tubular fluid = decreased rate of K+ secretion
    - serum k+ rises 0.7 mEq/L for every decrease of 0.1 pH unit during acidosis
  3. aldosterone levels
    - affect K+ loss in urine
    - ion pumps reabsorb Na+ from filtrate in exchange for K+ from peritubular fluid
    - high K+ plasma conc stimulates aldosterone
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11
Q

hypokalemia serum potassium conc is ____

A

> 3.5 mEq/L

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12
Q

hypokalemia is generally due to ? (4)

A
  1. renal loss
    - diuretics, renal disease, elevated aldosterone or corticosteroids
    - bartter syndrome, liddle syndrome, gitelman syndrome
  2. GI loss
    - D/V
  3. poor intake
    - poor nutrition, inability to eat, potassium-free IV fluids
  4. transcompartmental shift
    - B-adrenergic agonists
    - insulin
    - alkalosis
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13
Q

clinical manifestations of hypokalemia

A
  • impaired ability to concentrate urine - polydipsia, polyuria
  • neuro:
    1. paresthesias
    2. paralysis
    3. irritability/confusion
    4. drowsiness
  • muscular symptoms
    1. weakenss
    2. fatigue/lethargy
    3. cramps/tenderness
  • GI symptoms
    1. constipation
    2. ileus
    3. abdominal distension
  • cardiac
    1. hypotension
    2. palpitations
    3. dysrhythmias
    4. weak, thready pulse

A SIC WALK
Alkalosis!!

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14
Q

what would you see in an EKG with hypokalemia

A
  1. slightly peaked P wave
  2. slightly prolonged Pr interval
  3. ST depression
  4. shallow T wave
  5. prominent U wave
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15
Q

management of hypokalemia

A
  1. for acute-severe hypokalemia
    - potassium replacement with oral/IV KCl - 10-20 mEq/hr UNLESS life-threatening
  2. chronic hypokalemia
    - increase potassium-rich foods
    - correct underlying, predisposing conditions where possible (ex. chronic metabolic acidosis)
    - oral potassium supplement if needed

always monitor closely!

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16
Q

hyperkalemia serum potassium conc is ___

A

> 5.0 mEq/L

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17
Q

hyperkalemia is generally due to? (3)

A
  1. excessive intake
    - PO intake, USUALLY secondary to excess IV administration
  2. inadequate elimination
    - CKD, adrenal insufficiency, meds that interfere with normal excretion
  3. release from intracellular fluid
    - cell damage, excessive/severe muscle contraction
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18
Q

____: hemolysis of sample, prolonged tourniquet time, traumatic stick

A

pseudohyperkalemia

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19
Q

clinical manifestatinos of hyperkalemia

A
  1. neuro:
    - parethesias
    - weakness
    - dizziness
    - drowsiness
  2. muscular:
    - weakness
    - cramps
  3. GI:
    -N/V/D
    - ABD cramps
  4. cardiac:
    - palpitations
    - dysrhythmias
    - cardiac arrest
    - hypotension
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20
Q

how would the EKG look for hyperkalemia

A
  1. wide, flat P wave
  2. prolonged PR interval
  3. decreased R wave amplitude
  4. widened QRS
  5. tall, peaked T wave
  6. depressed ST segment
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21
Q

management of hyperkalemia

A

depends on severity including presence or absence of ECG changes
1. ALL patients
- DC meds that increase potassium
- educate on low-potassium diet
- consider starting meds to reduce potassium
2. for present EKG changes/notably high potassium
- IV calcium gluconate
- IV insulin + glucose
- +/- inhaled albuterol therapy
- +/- urgent diuresis (if kidney dysfunction is present)

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22
Q

loop diuretics for hyperkalemia

A
  • bumetanide, furosemide, torsemide
    1. more potent than thiazides
    2. SE: hypokalemia, hypovolemia, hyponatremia, metabolic alkalosis, hypocalcemia - can see ototoxicity, allergic rxn, hyperuricemia

check labs!

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23
Q

thiazides for hyperkalemia

A
  • hydrochlorothiazide (HCTZ), chlorthalidone, metolazone
    1. better tolerated
    2. SE: hypokalemia, hypovolemia, hyponatremia, metabolic alkalosis, hypercalcemia, PLUS hypomageniesemia - can asee hyperlipidemia, hyperuricemia, sleep disturbances

check labs!

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24
Q

cation exchange agents for hyperkalemia

A
  1. patiromer - binds K+ in gut in exchange for Ca++
    - SE: hypokalemia, hypomagnesemia, constipation or diarrhea
  2. sodium zirconium cyclosilicate - binds K+ in the gut in exchange for Na+ and H+
    - SE: hypokalemia, edema - can bind to other meds in GI tract

BOTH contraindication for allergy to med

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25
Q

3 medication classes to manage hyperkalemia

A

diuretics
cation exchange agents
potassium binders

26
Q

potassium binding resin for hyperkalemia

A
  1. sodium polystyrene sulfonate - binds K in gut
    - TAKES 24 HRS TO LOWER
    - SE: hypernatremia, hypokalemia, hypocalemia, hypomagnesemia
    – SIGNIFICANT GI SE - constipation, vomiting, intestinal necrosis
    - CI: hypokalemia, allergy, neonatal age, bowel obstruction

watch labs and be aware how pts are taking!
NO LONGER WIDELY RECOMMENDED

27
Q

3 bone minerals

A
  1. calcium - 99% for bone, 25% in bone
  2. phosphorus - 85% for bone, 12% in bone
  3. magnesium - 50-60% for bone, 0.37% in bone
28
Q

____% of ECF calcium is bound to plasma proteins, especially to ____

A

40%
albumin
cannot pass from plasma to ECF/ICF

29
Q

___% of ECF calcium is bound to other substances: (3)

A

citrate
phosphate
sulfate
also stuck in plasma

30
Q

___% of ECF is UNBOUND

A

50%

31
Q

what are ionized calciums?

A
  • free to move between fluids as needed
  • considered the metabolically active form
32
Q

___ is found in settings of low serum albumin

A

pseudohypocalcemia

33
Q

20-30% of ECF Mg is bound to ?

A

proteins

34
Q

____ is synthesized in skin after UV exposure OR found in diet

A

vitamin D

35
Q

vitamin D becomes activated by processing in ___ and ____

A

liver and kidneys

36
Q

what increases Ca and P absorption from the intestine and is needed for normal bone formation

A

vitamin D

37
Q

what substances/hormones regulate calcium and magnesium balance

A
  1. vitamin D
  2. parathyroid hormone (PTH)
  3. calcitonin
38
Q

what is parathyroid hormone and what are its function

A
  • produced by parathyroid glands
  • released when serum calcium lvls are LOW
  1. promotes release of Ca from bone
  2. increases activation of vit D
  3. stimulates renal calcium conservation and phosphate excretion
39
Q

___ is an important cofactor in synthesis and release of PTH

A

magnesium

40
Q

what is calcitonin

A
  • produced by thyroid
  • released when serum calcium levels are high
  • acts in opposition to PTH
41
Q

functions of calcium (5)

A
  1. muscular and neural activities
  2. blood clotting
  3. enzymatic rxns
  4. second messengers
  5. generation of AP
42
Q

functions of magnesium (5)

A
  1. enzymatic rxn
  2. ATP generation
  3. calcium transport
  4. potassium reabsorption
  5. PTH release
43
Q

which is more rare and is more often seen in critically ill patients - hypo or hypercalcemia

A

hypocalemia

44
Q

potential causes of hypocalcemia (4)

A
  1. impaired ability to mobilize stored calcium - hypoparathyroidism, hypomagnesemia, resistance to PTH
  2. decreased intake or absorption - vit D deficiency, malabsorption
  3. abnormal renal losses - CKD
  4. increased binding/chelation
45
Q

clinical manifestations of hypocalcemia

A
  1. nerve cells have decreased thresholds
  2. neuro:
    - anxiety, irritability
    - seizures
    - hyperactive reflexes
    - paresthesias - ESPECIALLY perioral
    - death!
  3. muscular:
    - cramps
    - laryngeal spasm
    - carpopedal spasm
    - chvostek sign
    - trosseau sign
  4. cardiac:
    - dysrhythmias
    - prolonged QT interval on ECG
  5. skeletal:
    - osteomalacia
    - bone pain
    - deformities
    - fracture

CATS - convulsions, arrhythmias, tetany, stridor and spasms

46
Q

management of hypocalcemia

A
  1. acute
    - IV infusion of calcium solution
  2. chronic
    - calcium replacement
    - vit D supplementation may be helpful
    - synthetic PTH preparations are available
47
Q

hyper calcemia serum calcium concentration ___

A

> 10.5 mg/dL

48
Q

serum calcium concentration can be falsely elevated in ____

A

prolonged draws with very tight tourniquet

49
Q

possible causes of hypercalcemia (3)

A
  1. increased bone resportion - hyperparathyroidism, cancer
  2. increased intake or absorption - excessive vit D or calcium, milk-alkali syndrome
  3. decreased renal elimination - thiazides, lithium
50
Q

clinical manifestations of hypercalcemia

A
  1. nerves have increased thresholds for excitation
  2. neuro:
    - lethargy
    - personality and behavior changes
    - diminished reflexes
    - coma
  3. muscular:
    - weakness/low tone
    - muscle atrophy
  4. skeletal:
    - bone pain
    - osteopenia/osteoporosis
  5. GI
    - anorexia
    - N/V/constipation
  6. renal:
    - inability to concentrate urine - polyuria, polydipsia
    - flank pain
    -kidney stones
  7. CV
    - shortened QT interval on ECG
51
Q

management for hypercalcemia

A
  1. hydration
  2. increasing renal excretion of calcium - loop diuretics
  3. limit release of new calcium from bone stores - bisphosphonates, calcitonin
  4. dialysis
52
Q

hypomagnesemia serum Mg concentration ___

A

<1.8 mg/dL

53
Q

hypomagnesemia is usually seen in combo with ___ and/or ____

A

hypokalemia
hypocalcemia

54
Q

causes of hypomagnesemia

A
  1. impaired intake/absorption - malnutrition/alcoholism
    - meds: PPI, loop diuretics
  2. increased Mg loss - diuretics, severe burns, hyperparathyroidism, hyperaldosteronism, diabetic ketacidosis
55
Q

kidneys are not great at preventing ____ loss

A

magnesium

56
Q

clinical manifestations of hypomagnesemia

A
  1. nerve cells have decreased thresholds for excitations
  2. neuro:
    - personality change
    - anxiety, depression, apathy
    - tremor
    - nystagmus
    - seizures
    - DEATHH
  3. muscular:
    - weakness
    - cramps
    - involuntary movements
    - tetany
    - babinski
    - chvostek
    - trosseau
  4. cardiac:
    - dysrhythmias
    - tachycardia
    - prolonged QT interval
57
Q

management of hypomagnesemia

A
  1. acute/severe
    - IV infusion of magnesium solution
  2. chronic
    - magnesium replacement - diet changes, oral supplements
58
Q

hypermagnesemia serum Mg concentration ____

A

> 3.0 mg/dL
rare

59
Q

causes of hypermagnesemia

A
  1. excessive intake - oral supplements, IV magnesium
  2. decreased excretion - AKI, CKD
60
Q

clinical manifestations of hypermagnesemia

A
  1. increased thresholds for excitation
  2. muscular:
    - weakness/low tone
    - flaccid paralysis
  3. CV:
    - bradycardia
    - hypotension
    - shortened QT interval
  4. neuro:
    - lethargy
    - confusion
    - diminished reflexes
    - coma
61
Q

management of hypermagnesemia

A
  1. DC magnesium therapy - IV calcium antagonizes magnesium
  2. dialysis if AKI/CKD PRESENT

MOD 3 (5 decks)

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