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
2
Q
_____ is generally impermeable to potassium
A
cell membrane
3
Q
potassium that leaves the cell is transported back inside by ____
A
Na/K/ATPase pump
4
Q
Potassium plays a key roll in what 2 main things?
A
- muscle cell excitability
- nerve impulses
5
Q
Potassium helps with ____ by being exchanged for H+ ions by kidneys
A
acid-base balance
6
Q
what 3 substances all cause movement from ECF to ICF
A
- insulin
- catecholamines
- B-agonist
7
Q
4 factors that promote lower serum potassium levels
A
- aldosterone
- insulin
- B-agonist activity
- alkalosis
8
Q
4 factors that promote higher serum potassium levels
A
- cell lysis
- strenuous exercise
- a-agonist
- acidosis
9
Q
potassium is regulated by activities of ion pumps, mostly distributed in the kidney:
A
- distal portions of nephron tubules and collecting system
- Na+ from tubular fluid is exchanged for either H+ or K+ in peritubular fluid
10
Q
3 factors responsible for urinary excretion of potassium
A
- changes in conc of ECF
- HIGH ECF conc INCREASES rate of secretion - 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 - 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
11
Q
hypokalemia serum potassium conc is ____
A
> 3.5 mEq/L
12
Q
hypokalemia is generally due to ? (4)
A
- renal loss
- diuretics, renal disease, elevated aldosterone or corticosteroids
- bartter syndrome, liddle syndrome, gitelman syndrome - GI loss
- D/V - poor intake
- poor nutrition, inability to eat, potassium-free IV fluids - transcompartmental shift
- B-adrenergic agonists
- insulin
- alkalosis
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!!
14
Q
what would you see in an EKG with hypokalemia
A
- slightly peaked P wave
- slightly prolonged Pr interval
- ST depression
- shallow T wave
- prominent U wave
15
Q
management of hypokalemia
A
- for acute-severe hypokalemia
- potassium replacement with oral/IV KCl - 10-20 mEq/hr UNLESS life-threatening - chronic hypokalemia
- increase potassium-rich foods
- correct underlying, predisposing conditions where possible (ex. chronic metabolic acidosis)
- oral potassium supplement if needed
always monitor closely!
16
Q
hyperkalemia serum potassium conc is ___
A
> 5.0 mEq/L
17
Q
hyperkalemia is generally due to? (3)
A
- excessive intake
- PO intake, USUALLY secondary to excess IV administration - inadequate elimination
- CKD, adrenal insufficiency, meds that interfere with normal excretion - release from intracellular fluid
- cell damage, excessive/severe muscle contraction
18
Q
____: hemolysis of sample, prolonged tourniquet time, traumatic stick
A
pseudohyperkalemia
19
Q
clinical manifestatinos of hyperkalemia
A
- neuro:
- parethesias
- weakness
- dizziness
- drowsiness - muscular:
- weakness
- cramps - GI:
-N/V/D
- ABD cramps - cardiac:
- palpitations
- dysrhythmias
- cardiac arrest
- hypotension
20
Q
how would the EKG look for hyperkalemia
A
- wide, flat P wave
- prolonged PR interval
- decreased R wave amplitude
- widened QRS
- tall, peaked T wave
- depressed ST segment
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)
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!
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!
24
Q
cation exchange agents for hyperkalemia
A
- patiromer - binds K+ in gut in exchange for Ca++
- SE: hypokalemia, hypomagnesemia, constipation or diarrhea - 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
25
3 medication classes to manage hyperkalemia
diuretics
cation exchange agents
potassium binders
26
potassium binding resin for hyperkalemia
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
3 bone minerals
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
____% of ECF calcium is bound to plasma proteins, especially to ____
40%
albumin
cannot pass from plasma to ECF/ICF
29
___% of ECF calcium is bound to other substances: (3)
citrate
phosphate
sulfate
also stuck in plasma
30
___% of ECF is UNBOUND
50%
31
what are ionized calciums?
- free to move between fluids as needed
- considered the metabolically active form
32
___ is found in settings of low serum albumin
pseudohypocalcemia
33
20-30% of ECF Mg is bound to ?
proteins
34
____ is synthesized in skin after UV exposure OR found in diet
vitamin D
35
vitamin D becomes activated by processing in ___ and ____
liver and kidneys
36
what increases Ca and P absorption from the intestine and is needed for normal bone formation
vitamin D
37
what substances/hormones regulate calcium and magnesium balance
1. vitamin D
2. parathyroid hormone (PTH)
3. calcitonin
38
what is parathyroid hormone and what are its function
- 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
___ is an important cofactor in synthesis and release of PTH
magnesium
40
what is calcitonin
- produced by thyroid
- released when serum calcium levels are high
- acts in opposition to PTH
41
functions of calcium (5)
1. muscular and neural activities
2. blood clotting
3. enzymatic rxns
4. second messengers
5. generation of AP
42
functions of magnesium (5)
1. enzymatic rxn
2. ATP generation
3. calcium transport
4. potassium reabsorption
5. PTH release
43
which is more rare and is more often seen in critically ill patients - hypo or hypercalcemia
hypocalemia
44
potential causes of hypocalcemia (4)
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
clinical manifestations of hypocalcemia
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
management of hypocalcemia
1. acute
- IV infusion of calcium solution
2. chronic
- calcium replacement
- vit D supplementation may be helpful
- synthetic PTH preparations are available
47
hyper calcemia serum calcium concentration ___
>10.5 mg/dL
48
serum calcium concentration can be falsely elevated in ____
prolonged draws with very tight tourniquet
49
possible causes of hypercalcemia (3)
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
clinical manifestations of hypercalcemia
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
management for hypercalcemia
1. hydration
2. increasing renal excretion of calcium - loop diuretics
3. limit release of new calcium from bone stores - bisphosphonates, calcitonin
4. dialysis
52
hypomagnesemia serum Mg concentration ___
<1.8 mg/dL
53
hypomagnesemia is usually seen in combo with ___ and/or ____
hypokalemia
hypocalcemia
54
causes of hypomagnesemia
1. impaired intake/absorption - malnutrition/alcoholism
- meds: PPI, loop diuretics
2. increased Mg loss - diuretics, severe burns, hyperparathyroidism, hyperaldosteronism, diabetic ketacidosis
55
kidneys are not great at preventing ____ loss
magnesium
56
clinical manifestations of hypomagnesemia
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
management of hypomagnesemia
1. acute/severe
- IV infusion of magnesium solution
2. chronic
- magnesium replacement - diet changes, oral supplements
58
hypermagnesemia serum Mg concentration ____
>3.0 mg/dL
rare
59
causes of hypermagnesemia
1. excessive intake - oral supplements, IV magnesium
2. decreased excretion - AKI, CKD
60
clinical manifestations of hypermagnesemia
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
management of hypermagnesemia
1. DC magnesium therapy - IV calcium antagonizes magnesium
2. dialysis if AKI/CKD PRESENT
