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patho ch 8 fluid
| Question | Answer |
|---|---|
| Sodium normal concentrations | 135-145 mEq/L |
| potassium normal concentrations | 3.5-5.0 mEq/L |
| Chloride normal concentrations | 98-106 mEq/L |
| Calcium normal concentrations | 8.5-10.5 mg/dL |
| Sodium Bicarbonate normal concentrations | 24-31 mEq/L |
| passive transport types | diffusion facilitated diffusion HIGH TO LOW |
| active transport | transport from high/low gradient using ATP as energy source |
| Na/K pump | active transport pump to bring intracellular sodium out and extracellular potassium in remember "K im out" -> K is brought out |
| intracellular and extracellular totals by % | intracellular is 40% total water in body extracellular is 20% total water in body |
| extracellular fluid by composition | comprises of 20% total body weight 14% interstitial 5% plasma 1% transcellular |
| hydrostatic pressure | pushing force, in arterioles (capillaries) hydrostatic PSI > osmotic PSI |
| osmotic pressure | pulling force in venules (capillaries) osmotic PSI > hydrostatic PSI |
| filtration | hydrostatic pressure force fluid from intravascular space into interstitial space |
| reabsorption | osmotic pressure pulls fluid from interstitial space back into intravascular space |
| colloid osmotic pressure | pressure induced by proteins (ie. albumin) in blood plasma |
| how is fluid balance regulated | thirst Renin-Angiotensin-Aldosterone system (RAAS) system antidiuretic hormone (ADH) diuretics |
| what are baroreceptors stimulated by | decreased arterial BP, ie in carotid artery/aorta |
| how is ADH stimulated | ADH production stimulated in hypothalamus by osmoreceptors detection of decreased blood volume/increased plasma osmolality AND ADH release from posterior pituitary storage |
| what does baroreceptor simulation do | cause increased sympathetic discharge (sympathetic activity) leading to decreased renal perfusion (vasoconstriction of renal vascular system) |
| tonicity is affected by | concentration gradients, water moves from low to high |
| isotonic | balanced concentration gradient |
| hypotonic | water in to cell, low extracellular gradient |
| hypertonic | water outside of cell, high extracellular gradient |
| what does the RAAS system do | regulate fluid balance and blood pressure (both are related) |
| renin | renal hormone which converts angiotensinogen to angiotensin |
| what are the types of baroreceptors | arterial baroreceptors (carotid/aortic baroreceptors) low pressure baroreceptors |
| what is ACE and what does it do | angiotensin converting enzyme converts angiotensin I to angiotensin II |
| omsoreceptors | receptors in hypothalamus that promote thirst |
| what are osmoreceptors activated by | activation by cellular dehydration (increased EC osmolality) or decreased blood volume |
| where does ACE primarily act in | the lungs |
| Angiotensin II function | regulates aldosterone |
| Aldosterone | hormone produced in adrenal cortex promote sodium retention and potassium excretion leading to increased BP |
| how does the RAAS system regulate BP and fluid balance | increase sodium and water reabsorption |
| hypovolemia causes | hemorrhage or dehydration |
| hypervolemia causes | water intoxication and edema |
| what does ADH do | increase renal H2O reabsorption/decrease urine excretion |
| 4 mechanisms of edema | increased hydrostatic pressure increased permeability decreased colloid osmotic pressure lymphatic obstruction |
| hypoparathyroidism | cause low parathyroid hormone (PTH) leading to low calcium and high phosphorus |
| cirrhosis pathophysiology | interference of local blood flow (reduced) and hepatocyte damage/necrosis portal hypertension |
| clinical manifestations of cirrhosis | ASCITES abdominal discomfort/increased girth increased weight sodium retention (d/t portal HTN) or hyponatremia (decreased renal fn and increased fluid retention) renal failure |
| cirrhosis causes renal failure via | hepatorenal syndrome = severe renal vasoconstriction |
| cirrhosis diagnostic criteria | physical exam body weight abdominal girth measurement labs via ascitic fluid analysis, liver/renal function, cardiac function |
| treatment for cirrhosis | paracentesis diuresis (via diuretics) IV albumin (increase colloid osmotic pressure) |
| what does sodium do for fluid | high sodium = fluid retention low sodium = fluid loss |
| dehydration pathophysiology | alteration in fluid/electrolyte balance (sodium imbalance vs negative fluid balance) |
| causes of dehydration | decreased fluid intake increased fluid output (diarrhea) fluid shift between compartments (ascites) |
| 3 classifications of dehydration in regards to sodium | hyponatremic isonatremic hypernatremic |
| hyponatremic | sodium <130 mEq/L hypertonic fluid loss where fluid shifts from intravascular to extravascular |
| isonatremic | Na 130-150 mEq/L isotonic event with zero fluid shift, like in diarrhea where fluid and sodium equally lost |
| hypernatremic | Na >150 mEq/L hypotonic fluid shift where fluid goes from extravascular to intravascular |
| dehydration clinical manifestations | decreased level of consciousness longer capillary refill time dry mucous membrane/less or absent tears/depressed fontanel + sunken eye vital sign changes oliguria/anuria |
| oliguria | decreased urination |
| anuria | absent urination |
| dehydration diagnostic criteria | H&P exam for fluid intake/output urine/stool/vomiting/sweating (ways to lose fluid/electrolytes) nutrition labs |
| labs for dehydration | electrolytes, bicarbonate, BUN/Cr, blood specific gravity |
| treatment for dehydration | rehydration via oral/IV fluids correcting electrolyte imbalance |
| hypoparathyroidism pathophysiology | altered Calcium balance and high Phosphorus PTH deficiency |
| parathyroid gland function | produces parathyroid hormone when calcium is low |
| how does parathyroid gland negative feedback regulation work | PTH production when Calcium low parathyroid hormone mobilize calcium elevation of calcium leads to reduced hormone production |
| parathyroid hormone | PTH moves calcium from storage sites such as the bone and enhances renal reabsorption of calcium |
| clinical manifestations of hypoparathyroidism | integumentary disorder (hair dry/loss, nail ridge/breakage, skin dryness) bone loss tingling in extremities visual change muscle cramp/seizures fatigue |
| diagnostic criteria of hypoparathyroidism | medical/surgical Hx physical exam lab test for PTH, calcium, phosphorus, magnesium, urine calcium |
| what can cause hypoparathyroidism | surgical damage to gland radiation autoimmune cause congenital cause |
| hypoparathyroidism tx | calcium supplement (carbonate/citrate) vit D supplement (calcitriol) recombinant parathyroid hormone |
Created by:
sleepingbear
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