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32 Cards in this Set
- Front
- Back
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What is ADH?
Where does it come from? What does it do? |
antidiuretic hormone is produced in the hypothalamus and released from the posterior pituitary. It's main roles are water retention (via increasing renal reabsorption) and increasing blood pressure (via vasoconstriction)
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What are different ways that stimulates ADH to be released to retain water?
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- pressure receptors in blood vessels detect hypovolemia
- osmoreceptors in hypothalamus detect hyperosmolarity - angiotensin II - sympathetic stimulation |
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ADH aka?
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vasopressin
arginine vasopressin |
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ADH vs aldosterone function?
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ADH --> increase water permeability in distal convoluted tubule.
Aldosterone --> increase in sodium retention. both result in water reabsorption, and increase in blood pressure. |
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Vasopressin vs aldosterone function?
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ADH --> increase water permeability in distal convoluted tubule.
Aldosterone --> increase in sodium retention. both result in water reabsorption, and increase in blood pressure. |
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What does aldosterone do?
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increases Na reabsorption, (thus fluid reabsorption), and decreases K
= Na retention, K loss |
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Where and when is Renin released?
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Renin is released from the juxtaglomerular apparatus (kidney)
It is released when there is a decrease in renal perfusion (low perfusion to JGA) |
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Where are the constituents of the RAAS system synthesized?
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Renin - juxtaglomerular apparatus of kidney
Angiotensin - Liver ACE - surface of lungs and renal endothelium Aldosterone - adrenal cortex |
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Explain the action of the RAAS system?
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in response to low BP (specifically, decreased renal perfusion), renin is relased from the kidneys. It converts angiotensinogen to angiotensin I, and ACE converts angiotensin I to active form angiotensin II. Angiotensin II increases BP and increases water reabsorption through a variety of mechanisms.
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What does angiotensin II do?
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1. sympathetic stimulation
2. tubular reabsorption of Na and Cl, H20 retention, and K excretion 3. aldosterone secretion (refer to 2.) 4. vasoconstriction 5. ADH secretion --> H20 absorption |
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What opposes the RAAS?
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ANP - atrial natriuretic peptide
decreases fluid volume and blood pressure |
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Why is creatinine and better indication of kidney function than BUN?
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creatinine is not affected by diet and normal physical exercise, liver disease
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What tests can tell you how well the kidney functions?
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blood creatinine level
creatinine clearance levels BUN levels |
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What lab results would indicate dehydration?
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high BUN:creatine
high BUN high urine specific gravity high serum osmolality |
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What is an important gerontological consideration when administering IV fluids to elder patients?
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rapid infusion is more likely to cause fluid overload, then cardiac failure for elderly patients.
bc of reduced renal function, reduced cardiac function |
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What are the normal values for electrolytes in the ECF?
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Na - 135-145 mEq/L
K - 3.5 - 5.0 Ca - 4.5 - 5.5 Mg - 1.5 - 2.5 Cl - 90 - 110 HCO3 - bicarb - 22-26 arterial, 24-30 venous |
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what is milk of magnesia?
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= magnesium hydroxide
used to treat short term constipation |
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What is the chief cation and anion of ECF and ICF?
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ECF - Na, Cl
ICF - K, HPO4 |
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Pt. has renal failure, and constipation. What is important for nurse to know when treating for constipation?
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Milk of Magnesia or Maalox is used to treat constipation.
Renal failure patients become at risk for hypermagnesemia. |
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What are signs of early dehydration?
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headache
fatigue loss appetite flushed skin heat intolerance light headedness dry mouth/ eyes burning sensation in stomach dark urine with strong odor |
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What are signs of advnaced dehydration?
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difficulty swallowing
clumnsiness shriveled skin sunken eyes visual disturbances painful urination numb skin muscle spasm delirium |
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List routine lab values for the following:
CO2 BUN creatine protein glucose HbA1C |
CO2 - 24-35 mmol/L
BUN - 5-25 mg/dl creatine - 0.5 - 1.2 mg/dl protein - 6-8 g/dl glucose - 60-120 mg/dl HbA1c 4-6% |
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Explain alkolosis and acidosis effect on potassium levels.
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Alkalosis - H+ ions move out of the cells to corrrect pH, while K+ moves into cells --> hypokalemia
Acidosis - H+ ions move into cells to raise pH, while K+ moves out of cells --> hyperkalemia |
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WHat are some causes of hypokalemia?
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- potassium sparing diuretics
- loss of gastric fluid (suctioning, vomit) - loss of intestinal fluid (diarrhea) - hyperaldosteronism (inc K renal excretion) -poor intake |
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Clinical manifestations of hypokalemia?
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anorexia, nausea, vomiting
fatigue, muscle weakness, leg cramps, decrease bowel motility, paresthesias, dysrhythmias |
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Compare ECG findings for pts with hypokalemia vs hyperkalemia
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Hypokalemia - inverted or flat T wave (ischemia)
Hyperkalemia - peaked T for moderate, no P wave and wide QRS for extreme |
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WHat is the danger of taking non K sparing diuretics and digitalis?
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diuretic may lead to hypokalemia
hypokalemia increases sensitivity to digitalis, increasing chances of toxicity |
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Hypo or hyper kalemia is associated with cardiac arrest?
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hyperkalemia
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Why must salt substitutes be taken with care?
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contains K --> possible hyperkalemia
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Causes of hyperkalemia?
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- hyperaldosteronism (addison's disease)
- K supplements and salt substit - acidosis - tissue trauma (burns, severe infection, chemo therapy) |
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What is the highest concern for pts. with hyperkalemia?
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cardiac efects - cardiac conduction (arrest)
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Clinical manifestations of hyperkalemia?
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- cardiac arrest
- weakness and paralysis - flaccid quadriplegia |
