Exam 5 Flashcards
Factors influencing water distribution
-Gender
-Body mass
-Aging
What happens to the fluid compartments with aging?
We lose lean muscle mass as we age, and with that we lose the fluid associated with the intracellular space. We also gain fat, which doesn’t hold as much water as muscle
Sensible Losses
Fluid loss we can measure: urine, fluids we drink, wound drainage etc
Insensible losses
Fluid losses we cannot measure: hard stool
What are the 3 forces that help us maintain fluid balance?
- Hydrostatic: pushing force against capillary walls
- Osmotic: pulling force of water created by solutes (Na is the primary determinant of this
- Oncotic: the pulling force created by albumin. Albumin attracts water and sodium
Describe the fluid movement in capillaries
Arterial End: Hydrostatic is stronger than oncotic and intersititial hydrostatic, so fluid moves into cells here
Venous End: oncotic pressure and interstitial hydrostatic are stronger at this End, so fluid moves back into intravascular space
Describe what happens to fluid movement in a patient with liver cirrhosis
Liver cirrhosis causes albumin to leak into tissues. Albumin will draw water into tissues (ascites) and creates a higher oncotic pressure in tissues like the peritoneum, that arnt meant to have fluid in them. Only way to get rid of it is via pericentesis. This is called 3rd spacing
Describe the RAAS Pathway
Stimulated by low blood volume and low blood pressure (I believe barroreceptors in aorta pick up on this) kidneys will release renin (enzyme) that converts angiotensinogen into angiotonsin 1. Angiontensin 1 is converted to Angiotensin II, which narrows blood vessels and triggers the release of aldosterone.
Describe ADH secretion and regulation
ADH (vasopressin) is produced in the hypothalamus but released by the posterior pituitary in response to increased blood osmolality. It’s picked up by osmoreceptors in hypothalamus, and when released, it tells the kidneys to retain water, (aquporins inserted in collecting duct) , tells sweat glands to hold water, and causes vasoconstriction of arterioles to raise BP. This is a negative feed back system so ADH is stopped when blood returns to normal
Causes of Dehydration
-high plasma osmolality
-fluid loss
- reduced ADH production (basically your not preventing water loss; also this can be caused by a tumor)
Dehydration symptoms
“TOD POT + WL”
-Tachycardia
-Orthostatic Hypotension
-Dry mucous membranes
-Poor turgor
-Oligourea
-Thirst
-Weight Loss
Dehydration Nursing Implications
Assess:
-Skin Turgor
- Intake and Output
-Urine color and quality
-Specific gravity >1.025
-Labs: BUN will be high
Edema Causes
-increased venous hydrostatic pressure (fluid doesn’t return to circulation)
-Low plasma oncotic pressure: not strong enough to pull fluid back into vessel –> CKD, liver issues, not enough protein
-Increased oncotic pressure in interstitial. 3rd spacing
Edema Symptoms
-High BP
-Peripheral Edema
-Polyurea
-Weight gain
-Lung Crackles, SOB
Edema Nursing Implications
Assess :
-extremities
-lungs and heart
-BP
-Intake and Output
-urine color and quantity
-specific gravity <1.010
-Labs
Third Spacing causes
-Liver Disease
-Low Albumin Levels
3rd Spacing Symptoms
-hypotension: fluid not in vessel anymore
-reduced urine output : no fluid going to kidneys
-edema
**Do not administer albumin if they have portal hypertension–> rupture **
Functions of the Kidney
-Maintains Fluid and Electrolyte balance
-Acid Base balance
Secondary function:
-produces erythropoetin
-produces Renin
-conversion of vitamin D into calcitriol
Furosemide Indications and MA
-targets loop of Henly where 20-25% NaCl and Water is reabsorbed stops this
-also activates renal prostaglandins –> vasodialation/ perfusion
Used to treat heart failure, liver disease, HTN (not first choice) and CKD by preventing passive reabsorption of water which reduced BP, vascular resistance, and venous return
Furosemide Adverse Reactions
-Hypotension
-Na and K depletion
Geri most at risk bc muscle mass loss
Thiazide Diuretic MA
-Acts on the distal convoluted tubule where 10% of NaCl, K and Water are reabsorbed.
-produces less diarhesis
-osmotic water loss
- may relax arterioles
HCTZ indications
-first choice for HTN
-adjunct treatment for HF, liver disease (with LD there’s a risk of portal hypertension)
-not much K lost here, so there may not be supplemental K given
HCTZ Adverse Effects
-electrolyte imbalance
-hypokalemia
Aldosterone significance
-part of the RAAS
-secreted by adrenal gland when BP is low
-acts the distal convoluted tubule and collecting duct to promote reabsorption of Na and water and DUMPS K to raise BP
Potassium Sparing Duiretic
-aldosterone antagonists
-prevents the reabsorption of sodium and water (10%) at DCT and CT and retains K
-used in conjuction with Furosemide or HCTZ
Spironolactone Indications
-HTN
-Counteract K loss with other diuretics
-treatment of edema related to HF, CKD, LD
Spironolactone Adverse reactions
-Hyperkalemia
Osmotic Duiretics (Mannitol)
-targets proximal convoluted tubule where 65% NaCl is reabsorbed and descending loop
-passively blocks reabsorption
-the increased osmotic forces cause rapid diarhesis (dehydration)
-Last resort for HTN, HF- Only used in ICU
Mannitol indications
-high intercranial pressure
-edema not relieved by other meds
Adverse Rxn
-Dehydration