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nursing > 2450 electrolytes (wk5) > Flashcards

2450 electrolytes (wk5) Flashcards

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1
Q

4 major cations

A

Na+, K+, Ca+, Mg+

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2
Q

3 major anions

A
  • bicarbonate HCO3-
  • chloride Cl-
  • Phosphate PO4-
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3
Q

3 major roles of Na+

A
  • h2o balance
  • conduction of nerve impulses w/ K+ & Ca+
  • membrane transport- carries other molecules
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4
Q

3 facts of Na+ h2o balance

  1. creates
  2. regulates
  3. when pumped out
A
  1. helps create osmotic pressure in ECF
  2. helps regulate BP
  3. when Na+ pumped out of cell, h2o (& chloride) follow
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5
Q

Na+ regulators & funx (3)

A
  1. aldosterone- renal reabsorption of Na+
  2. glomerular filtration rate- increase of GFR= increase loss of Na+
  3. natriuretic peptides: work in opposition to aldosterone, sodium wasting
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6
Q

hyponatremia range & causes (3)

A

less than 135

  1. Na+ loss (diuresis, burns, sweating, Gi loss hypoaldosteronism=addison’s dz)
  2. excess h2o (too much IV fluid, excess intake, increase intravascular fluid)
  3. fluid shifts (real failure i.e. high BUN, hyperglycemia)
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7
Q

hyponatremia manifestations (9) 4 seas go down

A
  1. h2o moves into cell ->cells swell
  2. abnorm cell membrane depolarization
  3. muscle cramps
  4. weakness, fatigue,
  5. confusion
  6. convulsions
  7. coma
  8. nausea
  9. decrease serum osmolality
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8
Q

hypernatremia range & causes

A

> 147

  1. h2o loss or decrease intake of h2o (watery diarrhea, fever, resp infx)
  2. excessive intake of Na+ or no loss of Na+ (hyperaldosteronism: pt holds onto too much Na+ and cannot get rid of it)
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9
Q

hypernatremia manifestations (i’d thirst)

A
  • h2o moves out of cell: cells shrink
  • h2o/Na+ imbalance (thirst, dry skin, mucous membrane, restlessness, seizure)
  • if caused by fluid loss: decrease BP, thready HR, increase temp
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10
Q

Potassium norm. range & major roles

  1. major… in ICF
  2. maintains…
  3. activates…
A

3-5

  1. major cation in ICF, maintained by NA/K ATPase pump
  2. maintains electroneutrality inside and outside cell with H+ during pH change
  3. Activates enzymes
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11
Q

3 facts about K+ being major cation in ICF

  1. how is K+ released
  2. maintains…
  3. important for 3 things
A
  1. when cells lyse K+ released
  2. maintains resting potential of cell membrane (with Na+)
  3. important for nerve impulses, cardiac rhythm, skeletal & smooth muscle
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12
Q

2 facts about K+ electroneutrality

A
  1. acidosis- excess H+ in ECF shifts into ICF, enters ecf

2. Alkalosis: H+ depleted in ECF and shifts out of ICF, K+ leaves ecf

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13
Q

3 facts K+ enzymes

  1. Na+/K+ ATPase pump is…
  2. K+ activates…
  3. Describe K enzymatic axn on stomach
A
  1. Na/K ATPase pump is required for glucose and glycogen movement into/out of cells
  2. K activates pyruvate kinase –> glycolysis (CHO metab)
  3. Gastric H/K ATPase pump in the stomach’s parietal cells is a proton pump that acidifies the stomach fluid (irritating to stomach)
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14
Q

K+ regulators & 3 facts

  1. Function of 1st K+ regulator
  2. Function of 2nd & 3rd regulator
  3. type of ion
A

1.Aldosterone: causes K+ secretion by distal tubules & sweat glands
2. insulin, epinephrine: both stimulate NA/K ATPase pump, moving K into cells
3. obligatory ion in kidney, faster the urine flow, the more K excreted
.

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15
Q

RAAS describe system (4)

  1. trigger
  2. release
  3. reaction
  4. result
A

Renin-Angiotensin-Aldosterone System

  1. Low BP/Volume is detected and causes Renin to be released in kidney
  2. Angiotesiongen causes release of angiotensin 1 –> angiotensin 2
  3. ateriole constriction —>negative feedback & adrenal cortex releases aldosterone
  4. NA+ reabsorption & h2o rentention in kidneys which increase BP & Volume
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16
Q

Natruiretic peptides 4 types & action (4)

  1. effect on volume
  2. reaction
  3. result
  4. 2 things also affected
A

Atrial, Brain, C-type natriuretic Peptide and Urodilantin (ANP, BNP, CNP)

  1. increase circulating volume (over time)
  2. secretion of peptides
  3. decrease reabsorption of Na+ & h2o in renal tubules and Na+ excreted
  4. also decrease in renin & increase GFR
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17
Q

Hypokalemia range & critical value & 3 causes

A

<3.5 less and less than 2.5

  1. insufficient intake
  2. excessive loss (diarrhea, diuretics, laxatives
  3. transcellular shift (excessive insulin or epinephrine or metabolic alkalosis)
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18
Q

hypokalemia manifestations 4

A
  1. N/V, ab distension, decrease/no BS, anorexia
  2. muscles weakness, fatigue, cramps
  3. irregular pulse, postural hypotension
  4. decrease deposit of glucose and glycogen (caused by Na/K pump defect)
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19
Q

hyperkalemia range & critical value, mortality value & rate

A

> 5, critical >6.5
mortality value: 8 (cells cant funx)
mortality rate: 67%

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20
Q

6 catalyst of hyperK+ (underlying cause) & 1 reason why there would be false lab value for hyperkalemia

A
  1. renal failure (can’t urinate K+ out)
  2. aldosterone deficiency addison’s (lose Na+ & hold on to K+)
  3. excessive administration of K+ (drugs, IV K+, banked blood)
  4. tissue trauma, burns, crushing injuries, extensive surgery (cell lysis)
  5. transcellular shift (insulin deficit, so no insulin can carry K+ into cell, metab acidosis, increase H+ in ECF cause K+ to exit cell, b/c H+ wants to enter cell)
  6. hypoxia (Na/K pump ATPase pump fail)
  7. Hemolysis of blood sample during venipuncture
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21
Q

hyperK+ manifestations & underlying cause

A

weakness, paresthesia brady<3 arrest

-failure of membrane potential

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22
Q

3 regulatory “hormones” for Ca+, PO4-, and Mg+

A

PTH, Vitamin D, Calcitonin

23
Q

3 funx of PTH

A
  1. promotes resorption of Ca+ in BONE into ECF
  2. promotes reabsorption of Ca+ & Mg+ in KIDNEY into ECF and causes excretion of PO4- (in kidney)
  3. increase vitamin D activation in KIDNEY
24
Q

what cell does PTH affect that promotes Ca+ resorption

A

osteoclasts are monocytic derivatives (giant-sized) that engulf bone tissue, thus removing Ca+ Phosphorus salts

25
Q

2 funx Vitamin D (D for doodoo & decrease) in Ca, PO4, & Mg+ regulation

A
  1. increase absorption of Ca+ & PO4- in INTESTINE

2. decrease PTH release & allows Ca+ & PO4- to enter bone

26
Q

where is Calcitonin released, what does it do (2)

A

released from c cells in thyroid

  1. inhibits Ca+ & PO4- resorption (promote osteoblasts (builds up blasts) & inhibit osteoclasts (clashes with clasts))
  2. Opposes PTH (inhibits Ca absorption & reabsorption)
27
Q

Ca+, PO4-, and Mg+ relationship w/ PTH

A

decreased Ca+ levels increase PTH (direct correlation)
Increased PO4- levels increase PTH (indirect)
Mg+ affects PTH synthesis relase and axn
high Ca+ will cause PTH secretion to be cut off but increase calcitonin

28
Q

term for:

  1. Ca+ intestine ->blood
  2. Ca+ bone ->blood
  3. Ca+ kidney -> blood
A
  1. absorption
  2. resorption
  3. reabsorption
29
Q

Normal Ca+ levels, 3 forms in blood, which is active

A

8.5-10.5

Ionized (active), complexed (attached to citrate, phosphate, and sulfate), protein bound (mostly to albumin)

30
Q

Ca+ major roles (4)

A
  1. enzyme rxn (ER controls intracellular Ca+ flow into cytoplasm, Intracellular Ca+ is next step in many rxns)
  2. membrane stability & permeability (affects membrane potentials & glue for membrane integrity)
  3. nerve conduction (calcium channels trigger conduction and contraction)
  4. coagulation cascade
31
Q

hypocalcemia range & 4 causes

A

<8.5

  1. inability to mobilize calcium stored in bones
  2. increased binding of (inactive) calcium (drugs, blood, alkalosis)
  3. decreased absorption from GI tract
  4. Diuresis
32
Q

what causes inability to mobilize Ca+ stored in bones

A
  1. hypoPTHism
  2. thyroid surgery
  3. hypomagnesemia
33
Q

what causes binding of Ca+

A
  1. drugs (tetracycline)
  2. blood transfusions (citrate preservative)
  3. alkalosis: increase pH decrease H+ & excess HCO3 -> Ca+ binds to protein & other anions that H+ was bound to
34
Q

what causes decreased absorption from Gi tract

A
  1. insufficient vita. D

2. extreme dieting, diarrhea, laxative abuse, alcoholism

35
Q

hypoCa+ manifestations

A
  1. cramping
  2. parethesias
  3. tetany (b/c deficit of Ca+ not able to maintain resting potential)
36
Q

two types of muscles spasms assoicated with hypoCa+

A
  1. chvostek’s sign spasm of facial nerce when cheek is tapped
  2. trousseau’s sign carpopedal spasm with inflated BP cuff on arm
37
Q

hyperCa+ range & causes

A

> 10.5

  1. increased bone resorption due to neoplasms
  2. increased bone resorption due to hyperparathyroidism
  3. immobilization
  4. acidosis: decrease in pH Increase in H+ -> Ca+ is released from proteins & other anions
38
Q

hyperCa+ manifestations

A
  1. muscle flaccidity, weakness, lethargy
  2. constipation, anorexia N/V
  3. Bone pain
  4. kidney stones
39
Q

PO4- normal range, absorption site, what else is need for absorption

A

2.7-4.5
GI tract absorption
Vita. D needed

40
Q

What is PO4- an essential component of

A 
ATP
2,3 DPG (delivers o2 to tissues)
nucleic acids (DNA RNA)
cell membrane (phospholipids)
bones & teeth
41
Q

Normal range for product of Ca+ & PO4-,
result if product higher than normal range,
major role for PO4-

A

<70, potential for metastatic
calcifications in soft tissues
buffer for acid-base balance

42
Q

hypophosphatemia range & critical value & causes

A

<1

  1. decreased absorption from intestines or decreased intake
  2. high metabolic states (alcohol withdrawal cancer)
  3. diuresis
43
Q

manifestations of hypophosphatemia:

A
  1. altered neuromuscular funx & decrease energy

2. altered blood cell funx & rigid walls which causes hemolytic anemia

44
Q

hyperPO4- range & cause

A

> 4.5

cause: 1. failure to excrete (renal fail or hypoparathyroidism
2. increased intake (laxatives contain PO4-)

45
Q

hyperPO- manifestations

A 
tingling, cramping
increased neuromuscular excitability 
tetany
parethesias
chvosteks & trousseau
46
Q

magnesium normal range & 3 regulators, AKA

A
  1. 8-2.7 (sedative of nerves)
  2. gi intake
  3. gi & renal excretion
  4. PTH -> reabsorption of Mg+
47
Q

Mg+ major roles (3)

A
  1. enzymatic rxn
  2. maintains <3 rhythm, facilitates nervous & muscle functioning (muscles unable to relax w/o Mg+)
  3. balances electrolytes, may cause hypoCa+/hypoK+
48
Q

Mg+ 4 enzymatic rxns

A
  1. Na+/K+/ATPase pump
  2. Ca+ pump activity (competes for receptor sites) natural Ca+ channel blocker
  3. proton pump in stomach
  4. CHO protein & lipid metab.
49
Q

how does Mg+ cause hypoCa+ & hypoK+

A

decrease Ca+ by decreasing PTH

decrease K+ by altering Na+/K+/ ATPase pump

50
Q

hypoMg+ range & causes

A

<1.6

  1. impaired absorption from intestines, GI loses
  2. increase loss from kidneys (b/c of decrease PTH or diuretics)
  3. malnutrition & alcoholism
  4. over ingestion of calcium
51
Q

hypoMg+ manifestations

A 
personality changes
neuromuscular irritability (hyperreflexia, muscle cramps, tetany)
52
Q

when is tetany the most severe

A

when both Mg+ & Ca+ are deficient

53
Q

hypermagnesemia range & critical value when there are s/s, causes

A 
range >2.7
critical >4.5
causes 1. failure to excrete
2. increase laxative/antacid use
3. over replacement
54
Q

hyperMg+ manifestations

A
  1. muscle weakness
  2. sedation
  3. hypotension (b/c Mg+ competes for Ca+ binding sites in smooth muscle & heart which decrease BP & arrhythmias)

nursing (15 decks)

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