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114 Cards in this Set
- Front
- Back
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why are we concerned with homeostasis?
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water and sodium are associated with ecf volume and osmolarity
-disturbances in K+ balance can cause cardiac + muscle problems -calcium, H+, bicarbonate ions allhelp with pH |
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why is maintaining osmolarity so important?
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because water crosses most cell membranes freely
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what happens if ECF osmolarity increases as a result of salt intake?
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water moves out of the cells and shrinks
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what is needed for fluid and electrolyte balance?
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respiratory and cardiovascular systems in addition to renal and behavioral responses
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decreased blood volume leads to
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decreased BP
which triggers volume receptors in atria, carotid, and aortic baroreceptors -triggers homeostatic reflexes |
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if BP decreases it triggers 3 reflexes
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cardio
behavior kidneys |
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the cardio system does what when bp decreases?
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it increases CO by vasoconstriction
thus raising BP |
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the behavior reflex does what?
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thirst causes increased water intake
increases ECF and ICF volume thus raising BP |
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kidneys
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conserve water to minimize further volume loss
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water percentages
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50% in women
60% in men 2/3 inside cells 3/70 in plasma 11/70 in isf |
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water gain
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2.2 L/day in food and drink
.3 metabolism = 2.5 total |
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water loss
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urine 1.5
insensible water loss (skin+lungs) .9 feces .1 = 2.5 total |
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pathological water loss disrupts homeostasis how
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volume depletion of the extra compartment decreases BP which means tissue doesnt get adequate oxygen
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kidneys do what
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only conserve fluid
cannot restore lost volume |
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where is urine concentration determined?
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in the loop of henle and collecting duct
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diuresis is
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the removal of excess water in urine
kidneys put out very diluted 50 mosm urine |
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how do you get dilute urine?
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kidney must reabsorb solute without allowing water to follow by osmosis
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fluid leaving loop of henle is hyposmotic why
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because thick portion of ascending limb transports Na+, K+, and Cl- out but is impermeable to water thus casing hyposmotic solution
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vasopressin controls
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water reabsorption and is an antidiretic hormone
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with maximal vasopressin
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collecting duct is freely permeable to water, water leaeves by osmosis and is carried away by the vasa recta caps... urine is concentrated
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in the absence of vasopressin
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the collecting duct is impermeable to water and the urine is diluted
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vasopressin and aquaporins
AQP2 |
exocytosis inserts the AQP2 water pores into the apical membrane and the cell is permeable to water
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mechanisms of vasopressin action
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1) vasopressin binds to membrane receptor
2) receptor activates cAMP 2nd messenger system 3) cell inserts AQP2 water pores into apical membrane 4) Water is absorbed by osmosis into the blood |
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what stimuli control vasopressin secretion?
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plasma osmolarity- most potent stimulus is increase
blood volume blood pressure |
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what threshold number is needed for osmoreceptors to stimulate release of vasopressin
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280 mOsM need to be met to fire
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osmolarity greater than 280
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hypothalamic osmorecpt
interneurons to hypothalamus hypothalamic neurons that synthesize vasopressin vasopressin released collecting duct epith insertion of water pores in apical membrane increased water reabsorption to conserve water |
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countercurrent exchange systems
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require arterial and venous blood vessels that pass very close to each other, with their fluid flow moving in opposite directions
-reduces heat lost to environment |
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countercurrent multiplier
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filtrate in descending limb becomes more concentrated
-in ascending limb, pumps out na, k, cl, and becomes hyposmotic |
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blood in the vasa recta removes water
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leaving the loop of henle and functionally goes in the other direction of filtrate flow in the loops of henle
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water leaving the descending limb does what
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it is attracted by the high plasma osmolarity
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this increases the osmolarity of he medullary interstitium
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urea
nearly half the solute in the medullary interstitial fluid is urea |
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why does salt increase blood pressure?
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because too much sodium requires more water to keep ecf na+ concentration at 140 mOsM... 1.1 more liters of water increases volume of ecf thus raising bp
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if we do not add water but increase salt what happens to osmolarity
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it goes up to 307 causing drawing away of water from the cells, shrinking them and disrupting normal cell function
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why does salt raise osmolarity?
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triggers vasopressin secretion and thirst
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controls sodium balance?
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aldosterone
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the more aldosterone, the more
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na+ reabsorption
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primary location and target of aldosterone?
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last third of distal tube
target is principal cells |
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why is na reabs auto followed by water reabs?
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because proximal tubule epithelium is always permeable to water
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what controls physio aldosterone secretion from the adrenal cortex/
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increased ec k conc. and decreased bp
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what trophic hormone stimulates aldosterone secretion in most situations?
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angiotensin II ANG II
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RAAS pathways
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1) granular cells in aa of nephron secretes enzyme renin
2) renin converts an inactive plasma protein, ANG I 3) ACE converts it to ANG II 4) finally, at the distal nephron, aldosterone initiates reabs of na+ |
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ANG II does what to bp
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it increases it
-increases vasopressin secretion -stimulates thirst -one of the most potent vasoconstrictors known in humans -activation of angII receptors in the cardio center increases sympathetic output to the heart and blood vessels |
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what do you do to Co and vasoconstriction to increase BP
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increase them
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ANG II related strongly to ____ bp
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increasing BP
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what drugs are made to stop ANG II
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ACE inhibitors
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natriuretic peptides
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atrial
brain enhance na+ and water excretion -increase GFR, decrease nacl and water reabs in collecting duct |
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k+ balance is essential
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for maintaining a state of well-being
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K+ low conc
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hypokalemia
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optimal levels of k+ conc
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3.5-5
hypokalemia below 3 leads to muscle weakness |
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why we need gatorade?
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hyperkalemia is more dangerous K disturbance because cells arent able to repolarize fully and become less excitable, consider a golfer who is dehydrated because of weather
-if you drink water, you keep ecf volume normal but drop osmolarity of k and na conc causing muscle weakness |
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increased osmolarity and volume
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ingestion of hypertonic saline
-excretion of hypertonic urine is called for |
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increased volume, no change in osm
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ingestion of isotonic saline
-excretion of isotonic urine |
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increased volume, decreased osm
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drinking large amounts of water
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nc volume, increased osm
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eating salt without drinking water
-intense thirst, prompts water |
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nc volume, decrease osm
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led to gatorade
replacement of sweat loss with plain water |
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decreased vol, inc osm
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dehydration
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decreased vol, no change in osm
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hemorrhage
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decrease in both
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incomplete compensation of dehydration, but uncommon so ignored
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visit table 20-1
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page 660
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what do you do in response to severe dehydration
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you do not secrete aldostereon which would cause na reabs which could worsen the already-high osm
-dehydration has low vol but high osm |
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increased osmolarity and volume
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ingestion of hypertonic saline
-excretion of hypertonic urine is called for |
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increased volume, no change in osm
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ingestion of isotonic saline
-excretion of isotonic urine |
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increased volume, decreased osm
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drinking large amounts of water
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nc volume, increased osm
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eating salt without drinking water
-intense thirst, prompts water |
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nc volume, decrease osm
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led to gatorade
replacement of sweat loss with plain water |
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decreased vol, inc osm
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dehydration
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decreased vol, no change in osm
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hemorrhage
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decrease in both
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incomplete compensation of dehydration, but uncommon so ignored
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visit table 20-1
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page 660
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what do you do in response to severe dehydration
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you do not secrete aldostereon which would cause na reabs which could worsen the already-high osm
-dehydration has low vol but high osm |
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figure 20-18 homeostatic compensation for severe dehydration
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1) carotid and aortic baroreceptors raise blood pressure
2) decreased peripheral bp directly decreases GFR which conserves ecf volume by filtering less fluid into the nephron |
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dehydration continued
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3) paracrine feedback causes the granular cells to release renin
4) granular cells respond to decreased bp by releasing renin which ensures increased production of ang II |
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dehydration continued again
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5) decreased bp, decreased volume, increased osm, and increased ang II all stimulate vasopressin and the thirst centers of the hypothalamus
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vasopressin
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increases water permeability of the renal collecting ducts allowing water reabs to conserve fluid
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the net result of the cardio response, ang II, vasopressin, and oral intake of water is
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restoration of volume by water conservation and fluid intake
-maintenance of bp thru increased volume, increased co, and vasoconstriction -restoration of normal osm by decreased na reabs and increased water reabs |
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what are particularly sensitive to changes in pH
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enzymes and the nervous system
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acidosis
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neurons become less excitable and cns depression results
-kidneys excrete H+ and reabsorb K+ |
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alkalosis
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pH is too high and muscles begin to twitch
-kidneys reabsorb H+ and excrete K+ |
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H+ input into plasma pH via
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diet (fatty acids, aa) and metabolism (co2 and water)
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acid input v. base input?
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acid input is greater
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what is the biggest source of acid on a daily basis?
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production of co2 during aerobic respiration (not an acid because doesnt contain any H+)
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why does co2 from respiration take forever to convert into h and hco3
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because of large amounts of carbonic anhydrase
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___ is the single biggest source of acid input under normal conditions
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production of h+ from co2 and water
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pH homeostasis depends on
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buffers- first line of d,
lungs- ventilation 75% of disturbances kidneys- renal regulation of h and hco3 |
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buffer systems include
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proteins, phosphate ions, and hco3
-a buffer is a molecule that moderates but does not prevent changes in pH by combining with or releasing H -without a buffer, acid would go way too high |
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most important extracellular buffer is?
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large amounts of bicarbonate produced from metabolic co2
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hco3 v H+ concentration in plasma
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hco3 is 600,000x as concentrated
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according to the law of mass action
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any change in co2, h, or hco3 will shift the equation
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now suppose h+ is added to the plasma from some metabolic source such as lactic acid
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in this case plasma hco3 can act as a buffer
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the effects of ventilation on pH
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hypoventilation increases Co2 which shifts equation to the right
hyperventilation decreases co2 and shifts to the left |
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the kidneys handle 25% of compensation and alter ph in 2 ways
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directly by excreting or reabs H+
indirectly by changing the rate at which hco3 buffer is reabs or excreted |
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membrane transporters
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apical na-h antiport
basolateral na-hco3 symport h-atpase h-k-atpase na-nh4-antiport |
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what does the proximal tube do with h and hco3
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it secretes h and reabs hco3
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the 2 pathways by which bicarbonate is reabs in the proximal tubule
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1) converts filtered hco3 into co2 and back into hco3
-h+ is secreted from the pt into lumen in exchange for filtered na+ |
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proximal tubule h+ secretion and reabs of filtered hco3 steps
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secreted h combines with filtered hco3 to form co2 in the lumen
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3
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co2 diffuses into the tubule cell and combines with water to form h2co3 which dissociates to h and hco3
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4
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h created in step 3 is secreted, replacing the luminal h that combined with filtered hco3 in 2
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5
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hco is reabs
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a second way to reabsorb bicarb and excrete h comes from metabolism of aa glutamine
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glutamine is metabolized to ammonium ion and hco3
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7
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nh4 is secreted and excreted
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8
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hco3 is reabsorbed
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intercalated cells
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interspersed among the principle cells are responsible for acid-base regulation
-have high concentrations of carbonic anhydrase |
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two types of intercalated cells
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type a function in acidosis
type b function in alkalosis |
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type a
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h is excreted
hco and k are reabs |
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type b
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hco3 and k are excreted
h is reabs |
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acid-base problems are caused by either
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respiratory or metabolic origins
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respiratory origins
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change in pCO2 resulting from hyper or hypovent causes ph shift
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metabolic
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pH problem from non-co2 origin
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respiratory acidosis
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alveolar hypoventilation results in co2 retention and elevated plasma Pco2
increased H and HCO3 and decreased pH bc it is a respiratory problem, cannot use resp compensation |
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metabolic acidosis
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input of H exceeds H excretion
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metabolic acidosis
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increase in H+ ions directly which shifts equilibrium to the left increasing co2 levels and using hco3 buffer
but pCo2 decreases thanks to hyperventilation |
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respiratory akalosis
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occurs as a result of hyperventilation
-alveolar ventilation increases without a matching increase in metabolic co2 production -a decrease in co2 shifts the equilibrium to the left, both H and and hco decrease, pH increases |
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what is the primary cause for respiratory alkalosis
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excessive artificial ventilation
-because it is a respiratory cause, the only compensation available is renal |
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metabolic acidosis
2 common causes |
excessive vomiting of acidic stomach contents
excessive ingestion of bicarbonate-containing antacids -in both cases the H is decreased shifting the equilibrium to the right meaning that pco2 decreases and hco increases -renal response is hco3 excreted and h is reabsorbed |
