Week 6 - Review Flashcards
Electrolytes:
Two forming bones and teeth
calcium and phosphate
Electrolytes:
Three involved in nerve transmission
Sodium, Potassium, Calcium
Electrolytes:
Pumped out of RBCs in exchange with bicarbonate
Chloride
Electrolytes:
Maintains blood and ECF volume
Sodium or Chloride
Electrolytes:
Two cation cofactors
Calcium & magnesium
Electrolytes:
Major buffer for blood pH
Bicarbonate
Electrolytes:
Three involved in muscle contraction
sodium, potassium, calcium
Electrolytes:
The non-hydrogen component of the acid of our stomach
chloride
Electrolytes:
Important component of ATP and genetic material
Phosphate
Electrolytes:
Two electrolytes that exist in ionized & protein-bound from
Ca2+ & Mg2+
Electrolytes:
Electrolyte can shift out of cells during acidosis for (H+)
K+
Electrolytes:
Electrolyte important in blood clotting
Ca2+
Electrolytes:
Electrolyte important for maintaining cell volume
K+
What is the largest body fluid compartment?
Intracellular
What results from excess NaCl intake?
redistribution of body water towards solutes
Why do electrolytes have greater osmotic power than non-electrolytes?
Salts dissociate into their ions:
1 NaCL ➡ Na+ & Cl-
Having bigger impact on osmotic pressure
During severe dehydration why would consuming plain water be dangerous?
Loss of water & electrolytes has already occurred.
Intake of plain water would dilute body solutes even more throwing off electrolyte balance
What process maintains common intra & extracellular [electrolyte]?
Na+/K+ pump
What hormone regulates the above electrolytes?
Aldosterone
Can be stimulated to release by chemicals arising at the kidney
Renin
Can be released if K+ is too high
Aldosterone = mineral corticoid ➡Na & K controller
Can be initiated by chemical release from the juxtaglomerular apparatus in the kidney
Renin
Results in dilution of the plasma solute concentration
ADH
(not aldosterone)
Can be released if blood volume and pressure are too low
Renin
During alkalosis, cells can shift K+ and H+.
What direction do the ions move & what results?
- H+ shifts out of the cells
- K+ shifts in to correct alkalosis
- But hypokalemia results
If you are dehydrated &. then rehydrate too quickly with water, what happens at the fluid electrolyte level?
- Dilution of Na+
- Hypotonic hydration and slowing down of cells
What happens if the parathyroid gland is over or underproductive?
- High PTH = excess Ca2+ & hyperpolarization
- Low PTH = little Ca2+ & depolarization
What electrolyte imbalances could occur in hyper or hypoaldosteronism?
Hyperaldosteronism =
⬆Na+ ⬇K+
Hypoaldosteronism =
⬇Na+ ⬆K+
ECF K+ is normally low & is maintained by daily dietary intake.
What would major GI distress do to this balance?
(vomiting, diarrhea, or stomach pump)
Loss of K+ in ECF
Hypokalemia & Hyperpolarization
Alnumin can bind minerals (Ca) or (H+) but not both.
In acidosis or alkalosis what should be stimulated & what will result?
Acidosis = (H+) binds and calcium unbinds. Hypercalcemia leads to hyperpolarization
Alkalosis = (H+) unbinds and calcium binds.
Hypocalcemia leads to depolarization
Which is more excitable and depressive.
Acidosis vs Alkalosis
Acidosis = more depressive
Alkalosis = more excitable
Does this condition have:
CNS vasodilation or constriction?
Depression or hyperexcitability?
Respiratory Acidosis
Vasodilation in brain & edema
Depression due to edema (even though hyperkalemia occurs), LOC or coma
Does this condition have:
CNS vasodilation or constriction?
Depression or hyperexcitability?
Respiratory Alkalosis
Vasoconstriction in CNS & low BF
Hyperexcitability = due to H+ unbinding from albumin & Ca2+ bindng
Hypocalcemia = Hyperexcitability
Does this condition have:
CNS vasodilation or constriction?
Depression or hyperexcitability?
Metabolic Acidosis
Hyperkalemmia & GI distress…but
Depression in CNS as H+ binds to albumin & hypercalcemia results and depression
Does this condition have:
CNS vasodilation or constriction?
Depression or hyperexcitability?
Metabolic Alkalosis
Hypokalemia is depressive, but…
Hypocalcemia caused H+ release from albumin and calcium binding
Hyperexcitability
