Fluid, Electrolyte, And Acid-Base Balance Flashcards
K+, Mg2+, and PO43- are predominant electrolytes in…
Intracellular fluid
Angiotensin 2 Functions
1)vasoconstriction (constricts BF to kidneys limits its ability ti excrete water)
-keeps more water in blood to ⬆️BV and ⬆️BP
2)➕ adrenal cortex to release aldosterone
-kidneys keep Na+ and H2O in blood
-⬇️ urination
3)➕ posterior pituitary gland to release ADH
-➡️ kidneys keep water and ⬆️BV
-➕ thirst mechanism
Hypothalamus and ADH
Makes ADH
Posterior pituitary and ADH
Stores and secretes ADH
⬆️BV➡️ _ BP
⬆️BP
RAAS mechanism
1) ⬇️BV➡️ ⬇️ BP
2) juxtaglomerular cells: release Renin into blood circulation
3) liver responds: activates angiotensinogen➡️ angiotensin 1
4) angiotensin-converting enzyme (ACE): turns angiotensin 1➡️ angiotensin 2
5)angiotensin 2
-major vasoconstriction (constricts BF to kidneys, limits its ability to excrete water)
-➕adrenal cortex to release aldosterone
-➕ posterior pituitary gland to release ADH
Diuretic
Helps pt’s excrete excess fluids in the body
Thirst mechanism
1) ⬆️osmolality (plasma)
-⬇️fluids, ⬆️solute
2) hypothalamus osmoreceptors respond
-➕ADH release
-thirst sensation experienced
3) kidneys respond
-sense ADH
-ADH causes DCT and CD to transport water
-water is put back into bloodstream and NOT excreted via urine
4) water is retained
ANP
Hormone release by ♥️ cells due to atrial wall stretching
-works against angiotensin 2
-stops effects of aldosterone, ADH, and renin
Fixed Acid
“Non-violate”
An acid that cannot be easily expelled from the body through the lungs as gas
Ex. HCl
Normal pH range
7.35-7.45
Hypernatremia
Na+ excess: > 145mEq/L
Hypernatremia causes
-dehydration
-uncommon in healthy individuals
-may occur in infants, elderly, and any individual unable to indicate thirst
-may result from excessive intravenous NaCl administration
Hypernatremia consequences
-thirst
-CNS dehydration
-confusion
-lethargy
-coma
-⬆️neuromuscular irritability
-twitching
-convulsions
Hyponatremia
Na+ deficit: <135mEq/L
Hyponatremia causes
-solute loss
-water retention
-vomiting
-diarrhea
-burned skin
-gastric suction
-⬆️⬆️⬆️use of diuretics
-⬇️aldosterone (Addison’s)
-renal disease
-⬆️⬆️⬆️ADH release
-⬆️⬆️⬆️ H2O ingestion
Hyponatremia consequences
-neurological dysfunction due to brain swelling
-if body Na+ content is normal but water is excessive, the symptoms are the same as those of water excess
-mental confusion
-giddiness
-coma
-muscular irritability/twitching
-convulsions
-accompanied by water loss: ⬆️BV and ⬆️BP
Hyperkalemia
K+ excess > 5.5mEq/L
Hyperkalemia causes
-renal failure
-⬇️aldosterone
-⬆️⬆️⬆️intravenous infusion of KCl
-burns or severe tissue injuries that cause K+ to leave cells
Hyperkalemia consequences
-nausea
-vomiting
-diarrhea
-bradycardia
-cardiac arrhythmias and arrest
-skeletal muscle weakness
-flaccid paralysis
Hypokalemia
K+ deficit < 3.5mEq/L
Hypokalemia causes
-GI tact distrurbances
-vomiting
-diarrhea
-gastric suctions
-cushings syndrome
-inadequate dietary intake (starvation)
-hyperaldosteronism
-diuretic therapy
Hypokalemia consequences
-cardiac arrhythmias
-flattened T Wave
-muscular weakness
-metabolic alkalosis
-mental confusion
-nausea
-vomiting
Hyperphosphatemia
HPO42- excess > 2.9mEq/L
Hyperphosphatemia causes
-⬇️urine loss due to renal failure
-Hypoparathyroidism
-major tissue trauma
-⬆️intestinal absorption
Hyperphosphatemia and hypo phosphatemia consquencds
Clinical symptoms arise b/c of reciprocal changes in Ca2+ levels rather than directly from changes in plasma [HPO42-]
Hypophosphatemia
HPO42- deficit <1.6mEq/L
Hypophosphatemia causes
-⬇️ intestinal absorption
-⬆️ urinary output
-hyperparathyroidism
Hyperchloremia
Cl- excess > 105mEq/L
Hypercholemia causes
-dehydration
-⬆️retention or intake
-metabolic acidosis
-hyperparathyroidism
Hypochloremia
Cl- deficit < 95mEq/L
Hypochloremia causes
-metabolic alkalosis
-due to vomiting or excess ingestion of alkaline substance
- ⬇️aldosterone
Hypercalemia
Ca2+ excess > 5.2mEq/L
Hypercalemia cause
-hyperparathyroidism
-⬆️⬆️⬆️ Vit D
-prolonged immobilization
-renal disease (⬇️excretion)
-malignancy
Hypercalemia consequences
-⬇️ neuromuscular excitability leading to…
-cardiac arrhythmias and arrest
-skeletal muscle weakness
-confusion
-stupor
-coma
-kidney stones
-nausea
-vomiting
Hypocalemia
Ca2+ deficit <4.5mEq/L
Hypocalemia causes
-burns (Ca2+ trapped in damaged tissues)
-Hypoparathyroidism
-⬇️Vit D
-renal tubular disease
-renal failure
-Hyperphosphatemia
-diarrhea
-alkalosis
Hypocalemia consequences
-⬆️neuromuscular excitability leading to
-tingling fingers
-tremors
-skeletal muscle cramps
-tetany
-convulsions
-depressed excitability of the ♥️
-osteomalacia
-fractures
Hypermagnesemia
Mg2+ excess > 2.2 mEq/L
Hypermagnesemia cause
-rare
-renal failure when Mg2+ is not excreted normally
-⬆️⬆️⬆️ingestion of Mg2+-containing antacids
Hypermagnesemia consequences
-lethargy
-impaired CNS functioning
-coma
-respiratory depression
-cardiac arrest
Hypomagenesemia
Mg2+ deficit < 1.4mEq/L
Hypomagnesemia causes
-alcoholism
-chronic diarrhea
-severe malnutrition
-diuretic therapy
Hypomagnesemia consequences
-tremors
-⬆️ neuromuscular excitability
-tetany
-convulsions
The kidneys generate buffer that enter the bloodstream in…
DCT and CD
Avg. % of water in the adult body
60-70%
Suppose the ECF osmolality becomes too high. What hormone would most likely be release to correct this situation?
ADH
T or F: adh secretion can be stimulated by either blood osmolarity changes or bp changes in the heart or large vessels
True
Primary buffer in the plasma
HCO3- buffer system
⬆️in CO2 levels leads to what change in pH.
⬇️ pH
most important renal mechanism for regulating acid-base balance involves
Maintaining HCO3- balance: reabsorption of filtered HCO3- from urine back into blood
Which acid base imbalance would be cause by over accumulation of CO2 in the blood?
Respiratory acidosis
Which of the following does NOT serve as a source of acids in the body?
a) aerobic breakdown of glucose
b) CO2 in the blood
c) fat metabolism
d) ingesting of HCO3-
Ingesting of HCO3-
In order to buffer a strong acid into a weak acid, which has a less dramatic effect dramatic effect on pH, what chemical should be used as the buffer?
Weak base
Effects of PTH
-➕kidneys to transform Vit D to its active form
-⬆️ intestinal absorption of Ca2+
-to activate bone-digesting osteoclasts
⬆️levels of what hormone would result in ⬇️ in reabsorption in CD in kidneys?
ANP
What results from ⬆️ levels of aldosterone?
⬆️Na+ reabsorption
What type of intravenous intravenous infusion would you give to a runner who has collapsed after drinking too much water during the course of her marathon and why?
Hypertonic saline solution to pull water out of cell
Under normal circumstances, what method does NOT lead to water intake?
A) metabolism
B) beverages
C) osmosis
D) food
C. Osmosis
Which of the following would NOT be expected to occur as a result of dehydration?
A) edema
B) reduced urine flow
C) Hypovolemic shock
D) shrinkage of body cells
A. Edema
ECF osmolality becomes too high. What hormone would most likely be released to correct this situation?
ADH
Where are signs of change in osmolality, stomach stretch, and thirst monitored?
In the hypothalamus
Which of the following is NOT involved in triggering the thirst mechanism?
A) detection of ⬆️osmolality by osmoreceptors
B) ⬆️BP
C) ⬇️BV
D) dry mouth
B. ⬆️BP
Major cation in ECF
Na+
Major anion in ECF
Cl- and HCO3-
Major cations in ICF
K+ and Mg2+
Hypertonic solution
⬆️[solute] outside the cell than inside
-water leaves cell➡️cell shrivels
-⬆️osmolality
-⬇️H2O
Hypotonic solution
⬇️[solute] outside the cell than inside the cell
-water enters the cell➡️ cell bloats
-⬇️osmolality
Isotonic solution
= distribution of water
Why does the interstitial fluid have ⬇️proteins?
Capillary membrane has pores that allow solute through except for proteins➡️ proteins stay in plasma➡️⬇️proteins in interstitial fluid
Normal Arterial Blood Gas (ABG) values
-pH: 7.35-7.45
-PaCO2: 35-45 mmHg- respiratory
-HCO3: 22-26 mEq/L- metabolic
-PaO2: 80-100mmHg
Hyperventilation
⬇️CO2
Respiratory alkalosis
Hypoventilation
⬆️CO2
Respiratory acidosis
