Pathophysiology Exam #3 - University of Cincinnati
How does fluid movement work? - ANS-- Arterial end = capillary hydrostatic pressure = pushing
pressure ---> filtration
- Venous end = higher capillary oncotic pressure --> pulling pressure ---> reabsorption
What is edema? - ANS-accumulation of fluid into interstitial space
What causes edema? - ANS-1. increased capillary hydrostatic pressure (venous obstruction)
2. Decreased plasma oncotic pressure (losses or diminished production of albumin)
3. Increased capillary permeability (inflammation and immune response)
4. Lymph obstruction (lymphedema)
5. Sodium retention
Pathophysiology = increase in forces favoring fluid filtration from the capillaries or lymphatic
channels into the tissues.
A person with heart failure has edema in the lower legs and sacral area. The nurse suspects
this condition is due to a(n): - ANS-Increase in capillary hydrostatic pressure
What is the role of sodium in fluid balance? - ANS-Is the primary ECF cation.
Regulates the fluid balance
Key ion in transport of other ions across the membrane
Sodium and Chloride react the same (both go up, both go down) EXCEPT for bicarb
Regulates osmotic forces, thus water
Roles include: Neuromuscular irritability, acid-base balance, cellular reactions, and transport of
substances Is regulated by aldosterone and natriuretic peptides.
• 136-145mEq/L
What is the hormonal regulation of fluids? - ANS--It is mediated by aldosterone (first control of
sodium in the body)
-A mineralocorticoid steroid synthesized and secreted from the adrenal cortex
-increases the blood pressure and volume
• Influenced by both plasma concentrations of sodium and potassium in circulating blood
• Secreted when sodium levels are depressed, potassium levels increases, or renal perfusion is
decreased
• Acts on the distal tubule of the kidney to increase reabsorption of sodium.
• Leads to sodium and water reabsorption back into the circulation and potassium and hydrogen
secretion to be lost in urine
Explain the Renin-Angiotensin-Aldosterone System. - ANS-A negative feedback system
The second control of sodium in the body
,• Sympathetic nerve stimulation and decreased perfusion/blood pressure in the renal
vasculature leads to the release of the enzyme renin juxtaglomerular cells of the kidney
• Renin stimulates release of angiotensin I, inactive polypeptide, which is then converted to
angiotensin II by ACE in pulmonary vessels
• 2 major functions of angiotensin II
1. Stimulates the secretion of aldosterone
- Aldosterone stimulates reabsorption of sodium and water restoring fluid balance
2. Causes vasoconstriction
- Vasoconstriction rises systemic blood pressure restoring renal perfusion
• Restoration of sodium levels, fluid volume, and renal perfusion leads to inhibition of the release
of renin = negative feedback because end result is opposite of initiating stimulus
What are natriuretic peptides? - ANS-Third regulation of sodium in the body
They work opposite of RAAS system
Negative feedback system
• Hormones that include atrial natriuretic peptide (ANP) and brain natriuretic peptide
1. ANP produced by myocardial atria
- Urodilatin is ANP analog that is released by kidney cells with increased renal blood flow
2. BNP produced by myocardial ventricles, and
• Natural antagonist to RAAS
1. Decreases blood pressure
2. Increase sodium and water excretion
• Released when there is increased atrial pressure (increased volume); e.g.. CHF
• Decrease in BP decrease atrial pressure therefore inhibiting release of ANP and BNP
What is the role of the antidiuretic hormone (ADH)? - ANS-- Is released when there is an
increase in plasma osmolality, decrease in circulating blood volume, or decrease in BP which all
result in decrease atrial pressure and ultimately secretion of ADH
• Is also called arginine vasopressin.
• Increases water reabsorption.
1. Increases permeability of renal tubules and collecting ducts of kidneys
2. Reabsorption of water mediated by ADH then promotes restoration of blood volume
• Increase in blood volume returns to heart, increasing atrial pressure, ultimately stopping
release of ADH
,A person reports severe diarrhea for 2 days. The practitioner understands this stimulates a(n): -
ANS-Increase in antidiuretic hormone secretion
What is an isotonic solution? - ANS-Contains equal concentrations of solutes on both sides.
What is a hypotonic solution? - ANS-the solution has a lower solute concentration than the cell
-lysed cells
What is a hypertonic solution? - ANS-The solution has a higher solute concentration than the
cell
-shriveled cells
What are isotonic alterations? - ANS-Total body water change with proportional electrolyte
change (no change in concentration)
- Isotonic volume depletion (hypovolemia)
- Isotonic volume excess (hypervolemia)
What are hypertonic alterations? - ANS-1. Hypernatremia
• Serum sodium >147 mEq/L
• Related to sodium gain or water loss
• Water movement from the ICF to the ECF
• Intracellular dehydration
• Manifestations: Intracellular dehydration, convulsions, pulmonary edema, hypotension,
tachycardia
2. Hyperchloremia
• Serum chloride levels exceed 105mEq/L
• Occurs with hypernatremia or a bicarbonate deficit.
• Is usually secondary to pathophysiologic processes.
• No specific symptoms are associated with hyperchloremia
3. Water deficit
• Dehydration- isotonic dehydration
• Pure water deficits
-Are hypertonic dehydration. It is rare and seen in comatose and paralyzed patients
• Renal free water clearance
-Common cause is result of impaired tubular function or inability to concentrate urine, DI
• Manifestations = Tachycardia, weak pulse, and postural hypotension, Elevated hematocrit and
serum sodium levels, Headache, dry skin, and dry mucous membranes
What are hypotonic alterations? - ANS-Decreased osmolality in ECF
Hyponatremia or free water excess
, Hyponatremia decreases the ECF osmotic pressure, and water moves into the cell
1. Hyponatremia
-Serum sodium level <135 mEq/L
• Sodium deficits cause plasma hypoosmolality and cellular swelling
• Pure sodium deficits; low intake
• Dilutional hyponatremia - excess TBW in relation to total body sodium or shift of water from
ICF to ECF = mannitol
• Hypotonic hyponatremia - TBW exceeds increase in sodium although both are increased;
severe congestive HF, ARF
• Hypertonic hyponatremia - shift of water from ICF to ECF in cases of hyperglycemia,
hyperlipidemia, and hyperproteinemia
-Manifestations: Lethargy, headache, confusion, apprehension, seizures, and coma
2. Hypochloremia
- Is usually the result of hyponatremia or elevated bicarbonate concentration
• Serum <97mEq/L
- Some causes are: Vomiting, Metabolic alkalosis, Cystic fibrosis
3. Water Excess
• Caused by: Compulsive water drinking, causing water intoxication, Decreased urine formation,
Syndrome of inappropriate ADH (SIADH), ADH secretion causes water reabsorption
• Normally associated with hyponatremia (dilutional)
• Manifestations: Cerebral edema, muscle twitching, headache, and weight gain
What is hypokalemia? - ANS-A serum potassium level less than 3.5 mEq/L.
Causes:
• Reduced potassium intake
• Increased potassium entry into cell (like insulin)
• Increased potassium loss (like high aldosterone)
• Hyperaldosterone state
• Commonly seen with respiratory alkalosis
Manifestations:
• Membrane hyperpolarization causes: (making the inside of the cell more negative)
-Decreased neuromuscular excitability
-Skeletal muscle weakness
-Smooth muscle atony
-Cardiac dysrhythmias
-U wave on electrocardiogram (ECG)
What is hyperkalemia? - ANS-A serum potassium level that exceeds 5.1 mEq/L.
-Rare as a result of efficient renal secretion
