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24 Cards in this Set
- Front
- Back
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how many mols of H+ are released by daily metabolic processes?
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50-100 mmol into 15-20 L of extracellular fluid
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Normal concentration of H+ in the body
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40 nmol/L, at pH 7.4
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Metabolism of organic constituents other than carbon, hydrogen, oxygen (2)
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1. convert amino nitrogen to urea
2. convert sulphur in sulphydry (SH) groups of amino acids to sulphate |
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What 3 compounds are essential for H+ homeostasis?
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1. H2CO3
2. H20 3. CO2 |
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Which 2 organs coordinate H+ homeostasis?
How? |
1. Lung (adjusts extracellular CO2)
2. Kidney - controls extracellular HCO3-, using water and CO2. - gets rid of H+ |
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What is the H+ homeostasis equilibrium?
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H2O + CO2 -> H2CO3 -> H+ + HCO3-
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What is Ka?
What is pKa? |
Ka = [H+] [A-]
------------ [HA] The tendency of any acid, HA, to lose a proton and form its conjugate base A-, is defined by the equilibrium constant. The equilibrium constant = ionization or dissocation constant = Ka pKa is the -log of Ka. strong acids -> larger Ka weak acids -> smaller Ka |
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What are buffers?
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weak acid and conjugate base, enabling solution to resist changes in pH when small amounts of an acid or base is added.
- compensates partially an influx or removal of H+ - buffering capacity maximal when pH = pKa |
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Henderson-Hasselbalch equation
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Ka = [H+] [A-]
----------- [HA] pH = pKa + log [A-]/[HA] pH = pH - log [A-]/[HA] When [HA] = [A-], pH = pKa + log 1.0 = pKa |
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Name 3 important biological buffers, and where they are found
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H2PO4, in renal tubular fluid
Hb in the erythrocytes H2CO3 in extracellular fluids, and glomerular filtrate |
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Name 3 other biological buffers (besides HPO4 and H2CO3)
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1. nucleotides.
2. proteins with amino acids w. functional groups that are weak acids or bases. Histidine in Hb. 3. metabolites w. ionizable groups |
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3 reversible equilibrium between gaseous CO2 in lung and HCO3- in blood plasma
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1. pH of a bicarbonate buffer depends on H2CO3 and HCO3-
2. H2CO3 concentration depends on concentration of dCO2 (d means dissolved) 3. dCO2 depends on concentration of CO2 (pCO2) in the gasous phase |
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How does one control buffering compartments? (3)
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1. control CO2 by respiratory centre and lungs
- rate and depth of breathing - diffusion from capillaries into alveolar sac, down a concentration gradient 2. erythrocytes and role of Hb -CO2 + H20 catalyzed by carbonic anhydrase - deoxyhaemoglobin buffers H+ produced: histidine promotes O2 release under acidic conditions 3. control bicarbonate by the kidneys - produced by tubular cells and reabsorption of filtered bicarbonate |
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How do erythrocytes control pH during CO2 release?
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Release:
Chloride shift (rate-limiting step) HCO3- comes out of the erythrocyte |
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How do erythrocytes control pH during CO2 removal?
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Chloride comes out of RBC (rate-limiting step)
HCO3- enters cell |
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What is concentration of HCO3- in glomuerular filtrate in relation to plasma?
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same concentration.
renal mechanism reabsorbs all. |
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How does renal reabsorption of bicarbonate occur?
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1. Antiport transport: Na+ pumped out of glomerulus into tubule, H+ pumped out of tubule into glom. (keeps intracelular Na+ so there's a concentration gradient)
2. CO2 moves down concentration gradient. Carbonic anhydrase catalyses formation of H2CO3, which dissociates to form HCO3- which is taken up by cotransporter. |
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What enhances HCO3- uptake from renal tubular cells? (4)
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1. decrease pH
2. increase pCO2 3. decrease in K+ 4. decreased ECF volume |
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how much H+ do kidneys excrete a day?
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40-80 mmol of H+ per day.
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What happens if renal mechanism can't resorb HCO3- or excrete H+?
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acidosis
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describe renal hydrogen ion excretion
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0. H2CO3 -> H+ and HCO3-
1. ATPase secretes protons into glomerulus. 2. NH3 combines with H+ secreted into glom. This forms NH4+ (which can't diffuse back into renal tubular cells due to plasma membrane barrier) |
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Define deviation from normal pCO2.
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1. Decreased
acute respiratory alkalosis: decreased H+, increased pH 2. Increased acute respiratory acidosis: increase H+, decreased pH |
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Define deviation from normal HCO3-
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1. decreased
acute metabolic acidosis: increased H+ production or bicarbonate loss. Increased H+, decreased pH 2. increased acute metabolic alkalosis: loss of unbuffered H+ decreased H+, increased pH |
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consequence of dysregulation (7)
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poor vascular tone
failure of myocardial pump risk of arrhythmia weakening of skeletal muscles electrolyte imbalance delirium/coma impaired cellular respiration |
