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31 Cards in this Set

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What is TBW and how do you calculate it? What are factors that affect it?
TBW = 60 % of the body weight

Calculation:
Body weight x 0.6 = 70 kg x 0.6 = 42 L

Gender:
Males > Females

Body composition:
-Increase fat tissue mass --> Lower TBW

Age:
-highest in Newborns, in both sexes decreases with advancing age and obesity
What are some of the distributions of TBW?
ECF = 14 L, 20 % BW, 1/3 TBW

Interstitial fluid = 10.5 L, 15 % BW

Plasma = 3.5 L, 5 % BW

Transcellular compartment: 15 ml/kg of BW
-Pericardial, pleural, peritonial, synovial
-CSF, endolymph, intraocular

ICF = 28 L, 40 % BW, 2/3 TBW

Ions make up 95 % of solutes:
-electrically neutral
-more in ICF than ECF
-same osmolarity in ICF and ECF because many cellular ions are bound to proteins and are osmotically inactive
What are the Ionic compositions of the ICF, ECF?
ICF:
-anions are bivalent or mutlvalent (organic phosphates and proteins are principle electrolytes, protein binding of some electrolytes makes then osmotically inactive)
-K and Mg are the principle cations

ECF:
-majority univalent
-Na is principle cation
-Cl and bicarbonate are principle anions
What are characteristics of Plasma vs Interstitial fluid and Plasma vs ICF?
Plasma vs. Interstitial fluid:
-capillary endothelium is freely permeable to water and small solutes but not to larger solutes (proteins and lipids)
-increase concentration of proteins
-5 % increase in cations and 5 % decrease in anions due to proteins

Plasma vs. ICF:
-increase Na, Ca, Cl, HCO3
-Low K, Mg, HPO4, proteins, organic ions
What are characteristics of Osmotic pressure? What are Osmolarity and Osmolality?
force that is necessary to apply to the more concentration solution to prevent solvent migration (to stop osmosis)

number of particles dissolved in the unit volume of the solution

NOT related to size, MW or particles or chemical constitution of solution

Osmolarity:
-osmotically active substances per L of solution (Osm/L)

Osmolality:
-solute concentration per kg of solvent (Osm/kg)
What is the total osmolarity for the Plasma, interstial fluid, and ICF?
Plasma = 301.8 mOsm/L

Interstitial Fluid = 300.8 mOsm/L

ICF = 301.2 mOsm/L

Osmolarity of plasma is about 1 mOsml/L higher than Interstitial fluid due to colloid osmotic pressure created by plasma proteins
What are Iso, Hypo, Hyper Osmotic solutions?
Iso:
-similar concentraiton with the ECF (plasma = 280-300 mOsm/L
-contains 0.9 % solution of NaCl which is a physiologic solution
-5 % glucose solution

Hypo: (causes swelling)
-OP < 280 mm Hg

Hyper: (causes shrinking)
-OP > 300 mm Hg
What are Iso, Hypo, and Hypertonic solutions?
Isotonic - do not change cellular volume
-0.9 % solution of NaCl - physiological solution
-5 % glucose solution

Hypertonic - cause cells to shrink (higher EOP than plasma)

Hypotonic - causes swelling (lower EOP than plasma)
What happens in water intoxication?
Hypo-osmotic volume expansion

-Excessive water consumption, SIADH

-ECF becomes less concentrated than ICF

-Osmotic shift of water into cells: lowering ICF osmolarity, increasing ICF volume, swelling of the RBC

lead to lower plasma protein concentraiton (due to increase in ECF water)
How is thirst regulated?
Dehydration = lower saliva, increase blood osmolarity, decrease blood volume and pressure

saliva leads to dry mouth --> receptors in mouth stimulate thirst center in HT

increase in blood osmolarity signals osmoreceptors in HT --> stimulation of thirst center in HT

lower blood volume leads to increase renin --> ATII production --> stimulation of thirst center in HT

All these lead to thirst and increase water intake to increase TBW
What are some disturbances of blood sodium and chloride?
Hyponatremia:
reasons - low sodium intake, excessive water intake, aldosterone deficiency, diuretics, increase sodium loss due to vomiting or diarrhea
consequences - hypotension, coma, tachycardia

Hypernatremia:
reasons - water deprivation and dehydration, increase intake, hyperaldosteronism
consequences - thirst, hypertension

Hypochloremia:
reasons - similar to hyponatremia
consequences - alkalosis

Hyperchloremia:
reasons - similar to hypernatremia
consequences - acidosis
What is the Biological role of Potassium?
K is major ion determining RMP --> changes in K have marked effect on cell excitability

major ICF osmotically active cation

critical for enzyme activities

acid-base regulation

extracellular K is regulated by cellular buffering (uptake of K) and by renal excretion
What are some disturbances of Blood Potassium?
Hypokalemia:
reasons - excessive loss, low intake, hyperaldosteronism, diuretics
consequences - increase diuresis, shallow respiration

Hyperkalemia:
reasons - hypoaldosteronism, transfusion of hemolyzed blood, renal failure
consequences - ventricular fibrulation
What is the Biological role of Phosphate and its daily turnover?
bones, teeth
buffers
high energy compounds
DNA, RNA etc

1000 mg per day in det, 65-70 % absorbed in gut

urinary excretion (650 mg) is equal to gut absorption
What are some disturbances of Phosphate?
Hypophosphatemia:
Reasons - alcoholism, malnutrition, diabetes mellitus
consequences - delirium

Hyperphosphatemia:
reasons - renal failure, hypothyroidism, aldosterone deficiency
consequences - hypotension, altered mental function, anorexia
What is the biological role of calcium and daily turnover?
skeletal framework

hemostasis

action potential generation

exocytosis, pinocytosis

second messenger system for hormones

absorbs 35 % in GIT
absorption (350 mg) = excretion
What are some disturbances of Calcium?
Hypocalcemia:
reasons - low PTH, high plasma phosphate
consequences - hyperactive reflexes

hypercalcemia:
reasons - increase PTH, increase Vit D
consequences - polyuria, depression
What are some functions, distribution, and balance of Magnesium?
functions:
-muscular contraction
-glucose metabolism

distribution:
-50 % in skeleton
-Less than 1 % in ECF

balance:
-50 % absorption in GIT
What are some disturbances of Magnesium?
Hypomagnesemia:
reasons - decrease intestial absorption, increase utilization
consequences - delirium, memory loss

Hypermagnesemia:
reasons - renal failure, destruction of bones
consequences - hyperactive reflexes
What is Blood pH and what are some of the protein buffers?
blood pH = 7.35 (venous) - 7.45 (arterial)

Buffers:
composed of functional groups of AA
-Carboxyl group - acts as an acid, releases H+ when pH increases
-Amino Group - acts as a base, combines with H+ when pH falls
-reduced Hb - combies with H+
What is the Carbonic Acid-Bicarbonate buffer?
-Bicarbonate acts as a weak base

-Carbonic acid acts as a weak acid

-cannot protect against pH changes due to respiratory problems
What is the Phosphate buffer?
Components:
-Dihydrogen phosphate - a weak acid
-Monohydrogen phosphate - a weak base

plays an important role in buffering of ICF and urine
What happens in exhalation of CO2?
increase ventilation --> increase elimination of CO2 --> reaction driven to left --> increase in blood pH

decrease ventilation --> lower blood pH

negative feedback loops mediated by chemoreceptors
How is HCO3 reabsorbed after it is filtered and H+ secreted?
Kidneys reabsorb HCO3 and secrete H+

HCO3 reabsorption primarily occurs in proximal tubule and is coupled with H+ secretion

also occurs in collecting ducts (Typa A intercalated cells)
What is the transport mechanism of H+ secretion in the Nephron?
Primary active H-ATPase pump:
-apical membrane

Na+/H+ countertransport:
-the proximal tubule and thick ascending limb

H+/K+ countertransport:
-intercalated cells of collecting duct

Basolateral transport of HCO3 occurs through Cl-/HCO3 countertransport or Na/HCO3 cotransport
How do the intercalated cells handle H+ and Bicarbonate?
Reabsorption of H+:
-proton pump is located in baso-lateral membrane

Secretion of Bicarbonate:
-Cl/HCO3 countertransport is located in apical membrane
What is the process of the reabsorption of bicarbonate?
in the lumen:
-secreted H+ combines with filtered HCO3 to make H2CO3
-this H2CO3 then dissociates into CO2 and H2O catalyzed by brush border carbonic anhydrase

CO2 and H2O diffuse into the cell

Proximal tubule cells:
-H+ and HCO3 produced from CO2 and H2O
-combine to form H2CO3 by intracellular carbonic anhydrase
-H2CO3 dissociates into H+ and HCO3
-H+ is secreted therefore HCO3 IS REABSORBED

results in net reabsorption of filtered HCO3 but not not result in secretion of H+ (it is recycled)
What is the overall result of H+ secretion - Bicarbonate reabsorption?
-H+ ions which were secreted into the lumen and combined with HCO3 are not excreted into the urine, they are incorporated into H2O.

-Bicarbonate filtered from plasma is reabsorbed but HCO3 is NOT the same HCO3 that was filtered

-Adding of new HCO3 to plasma - renal excretion of acid; the secreted acid combines with other than HCO3 buffers is excreted
-addition of new bicarbonate to plasma is accompanied by excretion of equivalent amt of acid into final urine
How is H+ buffered in the Renal tubules?
HCO3

monohydrogen phosphate

NH3

Excretion of acid in urine
What are the 4 acid-base balance disturbances?
Metabolic Acidosis:
-low HCO3 leads to lowering of PCO2
-respiratory hyperventilation
-loss of bicarbonate due to diarrhea
-compensated by respiratory: hyperventilation which causes loss of CO2, pH will go normal but HCO3 will remain low

Metabolic Alkalosis:
-Respiratory hypoventilation
-high HCO3 leads to increase in PCO2
-loss of acid due to vomiting
-compensated by respiratory: hypoventilation leading to loss of CO2, HCO3 will remain high

Respiratory acidosis:
-increase PCO2 leads to increase HCO3
-caused by hypoventlation due to airway obstructions
-compensated by renal: increase excretion of H+ and reabsoprtion of HCO3, PCO2 will remain high

Respiratory alkalosis:
-decrease PCO2 leads to Decrease HCO3
-caused by hyperventilation due to O2 deficiency
-decreased excretion of H+ leading to decreased reabsorption of HCO3, PCO2 will remain low
What is the serum anion gap?
unmeasured anions in the serum

anions include phosphate, citrate, sulfate, and protein