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Biochem > Lecture 1- Acids, Bases and Buffers > Flashcards

Lecture 1- Acids, Bases and Buffers Flashcards

1
Q

Water Functions

A
  • Solvent for compounds in body (most important)
  • Helps transport molecules
  • Creates intra and extracellular enviro, constant enviro via homeostasis
  • Thermal regulation: distribution of heat in body, perspiration
  • Produced and Used in chemical reactions
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2
Q

Fluid Compartments in Body

A 
Intracellular fluid (ICF): ~60% of water contained in cells 
Extracellular fluid (ECF): Plasma-fluid portion of blood and Interstital fluid (IF)-fluid in spaces between cells
-ECFs also are lymph, eye humor and GI secretions
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3
Q

Negative Water Balance/Dehydration

A

-Water loss > water intake
Causes: -excessive sweating/diarrhea -Severe burns -Impaired kidney Fx
Signs/symptoms: -Cotton mouth -Dry/flushed skin -AMS -Fever

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4
Q

Dehydration Examples

A

Inadequate H20 intake: -pts that can’t swallow -loss of appetite -Brain injury causing loss of thirst
GI water loss-impaired reabsorption: Secrete 8-10L per day, normally is reabsorbed
High [solute] in urine: Osmotic diuresis ([ketone bodies] and [glucose] in urine), prevents reabsorption in kidneys

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5
Q

Hypotonic Hydration/Overhydration

A
  • Water loss < water intake
  • Water intoxication due to dilution of Na+ in ECF = hyponatremia. Causes tissue swwelling
  • Caused by increased water retention or decreased water excretion, often from renal insufficiency
  • Symptoms: nausea/comitting, cerebral edema, convulsions, coma, death
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6
Q

Edema

A

-Excessive fluid build up in Interstitial spce
Causes: -increase of fluid flow out of blood stream -decrease in fluid return
Contributing factors: -HTN -CHF -Decreased blood osmotic pressure -Impaired circulation

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7
Q

Ions in body fluids

A

ECF: Na+: 145 K+:4 Cl-: High Phosphate: low
ICF: Na+: 4 K+: 150 CL-: low Phosphate: High
*balance of ECF sodium and ICF potassium prevent net water movement

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8
Q

Acid- Base Balance

A
  • mostly maintained by proton concentration
  • Protons have big impact on biochem reactions, physio processes, homeostasis
  • Body maintains [proton] in blood, ICF, other places
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9
Q

Hydrogen Ion Sources

A 
-CO2 is major metabolic source of acid 
CO2 + H20 ->H2CO3 (carbonic acid) 
H2CO3-> H+ + HCO3-
-Catabolism of compounds w phosphorus = phosphoric acid in ECF 
-Glycolosis -> lactic acid 
-Fatty acid oxidation -> ketone bodies
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10
Q

Body pH maintenance

A
  • Buffers: act in seconds, bicarb, phosphate, hemoglobin
  • Respiratory Center: acts in minutes, removes H2CO3 (carbonic acid) by expiration
  • Renal system: takes hours/days to affect pH, major pH regulator
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11
Q

Metabolic Acids and Buffers

A 
-Acid needs to be buffered until it can be excreted in urine or expired 
Bicarbonate-carbonic acid: ECF
Hemoglobin buffer system: RBC 
Phosphate buffer system: all cell types 
Ammonium and phosphate ions: kidneys
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12
Q

Bicarbonate buffer system

A

CO2 + H20 (carbonic anhydrase) H2CO3 (carbonic acid) H+ + HCO3- (bicarbonate)

  • Most Co2 from TCA/krebs cycle
  • H2CO3 replenished from dissolved Co2
  • the more carbonic acid converted to H+ and bicarb, the more CO2 and H20 used to make carbonic acid
  • Dissolved CO2 in equillibrium w CO2 in lungs, amount of Co2 available is regulated by respirations
  • if pH falls, respirations increase to expire Co2
  • if pH rises, respirations decrease to retain CO2
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13
Q

Anion Gap

A
  • Difference in concentration of cations/anions in serum/plasma/urine
  • measured in mEq/L or mmol/L
  • [Na+] - ([Cl-] + [HCO3-]) (K+ is negligible so not included
  • Normal adult anion gap is 8-12 mEq/L
  • bigger gap indicates metabolic acidosis
  • low blood pH , means bicarb (HCO3-) and H+ will react to form more carbonic acid (H2CO3), means that [HCO3-] is low
  • so anion gap is low
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14
Q

Bicarbonate and Hemoglobin in RBC

A
  • CO2 from krebs/TCA -> interstital fluid -> blood plasma -> RBC
  • CO2 + H20 (carbonic anhydrase) H2CO3 (carbonic acid) H+ + HCO3- (bicarbonate) occurs in RBC
  • H+ binds to Hb -> HbH
  • HCO3- transported into blood in exchange for Cl- (raises acidity)
  • In lungs, CO2 is low
  • More CO2 is relased from RBC, so RBCs convert more H2CO3 to CO2 and H20, and more H+ and HCO3- converted to H2CO3
  • Hb loses some of H+ that allows it to bind O2 more readily
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15
Q

Intracellular pH

A
  • Major buffers are phosphate anions and proteins (except in RBC)
  • H2PO4- (Dihydrogen phosphate, has maximum buffering capacity at physiological pH) dissociates into H+ and HPO4– (hydrogen phosphate)
  • Glucose 6-phosphate, ATP, and proteins can accept H+ and act as buffers
  • Transport of H+ out of cell important for pH maintenance
  • Metabolism produces acids (ketones/lactic acid)
  • Metabolic anions transported out of cell w H+
  • if cell pH too low, more H+ exchanged for Na+
  • if cell pH too high, more HCO3- exchanged for Cl-
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16
Q

Urinary Hydrogen and Phosphate Ions

A
  • Nonvolatile (cant be expired) are excreted in urine
  • most nonvolatile acids buffer urinary pH at 5.5-7
  • urine secretes phosphate/ammonium ions, uric acid, di and tricarboxclic acids, (H2PO4- excretion reduces acidity)
  • Excreted phosphate =ingested phosphate, H2PO4- or HPO4– excretion in urine depends on blood and urine pH
17
Q

Ammonium as Buffer

A
  • Major contributor to buffering urinary pH (NOT blood)
  • Ammonia (NH3) is a base, NH3 + H+ NH4+
  • NH3 produced from AA metabolism/absorbed in GI and must be kept at low concentration bc is toxic
18
Q

Hydrochloric Acid

A
  • HCl/gastric acid secreted by parietal stomach cells, low pH denatures ingested proteins for digestion and kills most of ingested infection agents
  • Stomach content -> lumen of small intestines and neutralized by HCO3- (secreted by pancreas/intestinal lining)
19
Q

Metabolic Acidosis

A

Causes: -DKA -renal disease(protons retention) -lactic acidosis (tissue hypoxia from resp failure/cardiac arrest) -certain drug OD/poisoning
Lab results: High [H+}. low pH, low [pCO2], low [HCO3- ]
1. Increased H+ production = blood [H+] increase = low blood pH
2. H+ buffered by HCO3-
3. Hyperventilation to expire CO2

20
Q

Metabolic Alkalosis

A

Causes: -prolonged vomiting -K+ deficiency (K+ move out of cell in exchange for H+)
Labs: Low[H+}. High pH,High [pCO2], Low [HCO3- ]
1. Loss of H+ = blood [H+] decrease= highblood pH
2. Excess HCO3- produced to try to replace H+
3. Hypoventilation to increase CO2

21
Q

Respiratory Acidosis

A

Causes: -Choking -bronchopneumonia -acute asthma - COPD
Labs: High [H+}. low pH, high [pCO2], high [HCO3- ]
1. Insufficient expiration = high CO2
2. Blood [pCO2] increases -> favors carbonic anhydrase reaction to produce more H+ and HCO3-
3. Blood [H+} increases

22
Q

Respiratory Alkalosis

A

Causes: -Hyperventilation - high Intracranial pressure or hypoxia (stimulate resp. center)
Labs: Low [H+}. High pH, Low [pCO2], Low [HCO3- ]
1. Excessive expiration = low CO2
2. Blood [pCO2] decreases-> carbonic anhydrase favored to use up H+ and HCO3- to make more CO2

Biochem (14 decks)

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