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16 Cards in this Set

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  • Back
Filtration depends on a specific vital statistic - what is it?
Filtration is influenced by blood pressure
How is GFR altered by the body, over the short term?
If GFR gets too big, afferent arteriole is constricted to reduce blood flow to nephrons, letting GFR go down again
If GFR gets too small, afferent arteriole is dilated to increase blood flow to nephrons, letting GFR rise again
this process is called "local control" or "short term control"
How is filtration altered by the body, over the long term?
Long term control is the renin angiotensin cascade, to alter BP regulation, signaled by the juxtaglomerular apparatus in the kidneys
For long term, if GFR is too high, levels of renin will drop> angiotensin decreases> aldosterone decreases > less salt > less water > less pressure > less GFR
for long term low GFR, opposite process occurs
What kinds of substances are reabsorbed from urine? How is this accomplished?
Reabsorbed from urine (usually passive via enzymes, regulated by channels opening and closing)
Salt (passive, osmosis)
Water (passive, osmosis)
HCO3- (diffusion)
Glucose
Amino Acids
What substance is secreted into urine, making it increasingly more acidic? How is this accomplished?
Secreted into urine (usually active transport)
H+ (acid) (Active transport, normally)
What is the long term mechanism for changing H20 (water) reabsorption?
When H2O is excessive, ADH goes down > H2O channels close > reabsorption of H20 goes down = flush
When H20 is low, ADH goes up > H2O channels open > reabsorption goes up
What is the long term mechanism for changing Na+ (salts) reabsorption?
When Blood Na+ goes up, Aldosterone goes down > Na+ channels close > reabsorption of Na+ goes down
When Blood Na+ goes down, Aldosterone rises > Na+ channels open > reabsorption of Na+ goes up
How would urine/urinalysis change when a person has renal disease?
Renal disease = brownish urine, large molecules getting in urine
How would urine/urinalysis change when a person has diabetes melitus?
Diabetes melitus = glucose in urine (sustained, or after fasting), high osmolarity
How would urine/urinalysis change when a person has diabetes insipidus?
Diabetes insipidus = clearish and high volume urine, low osmolarity
What are ECF and ICF? How do they relate to IV fluids?
ICF (Intracellular fluid/cytosol)
ECF (Extracellular fluid) - Plasma, Interstitial fluid (between cells) = exchangable to small solutes, can go in or out of cell
Hypertonic (high salt) solution IV = Blood cells shrink (crenate)
Hypotonic (low salt) solution IV = Blood cells expand - prolonged excess may be signaled by pitting edema or inspiratory rales
secondary regulation of tonicity may be accomplished by sweating/thirst
What are alkalois and acidosis? How are they compensated for within the body?
Acidosis (high acid, low Ph(7.35-)) and alkalosis (high base, high Ph (7.45+)) may be regulated by chemical buffers (within seconds), breathing (within minutes, short term), or renal mechanisms (within hours or days, long term)
CO2 + H20 (Respiratory side) <> H2CO3 <> H+ + HCO3- (Renal/Metabolic side)
What is metabolic acidosis/alkalosis? How is it compensated for?
Metabolic acidosis/alkalosis (due to diet, breathing does opposite to compensate (breathes faster/slower))
What is respiratory acidosis/alkalosis? How is it compensated for?
Respiratory acidosis/alkalosis (due to breathing), renal system opposes to compensate (increased/decreased acidity in urine, decreased/increased reabsorption of acid)
How would having diarrhea alter body chemistry?
Diarrhea > Metabolic acidosis (due to increased feces (basic) leaving body), breathing rate increases to blow off excess acid
What are "normal" measured stats for pCO2 and HCO3-?
normal pCO2 35-45 mm Hg, normal HCO3- about 25 meq/liter