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Renal I > Test 2 (Renal Control of Acid-Base Balance) > Flashcards

Test 2 (Renal Control of Acid-Base Balance) Flashcards

1
Q

Importance of Maintaining pH

A
  • H+: Reactant or product of many Enzymatic Reactions; Affects Reaction Rate
  • Effects of H+ on net Electrostatic Charge of Proteins (Amphoteric): Affects Protein Function
  • Effects of H+ on Free Plasma Concentrations of other cations (EX: Ca2+)
  • Effects of H+ on Intracellular Cation Concentration (Na+/ H+, K+/ H+ Exchanger)
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2
Q

Chemical Buffer Systems

A
  • Mixture of WEAK ACID and its CONJUGATE BASE in aqueous Solution
  • Chemical buffers minimize but don’t completely prevent pH changes caused by STRONG ACID or BASE
  • Ability (“Strength”) of buffer to minimize pH Changes depends on:
    a) Concentrations of Buffer System Components

b) Nearness of Buffer’s pKa to pH of Solution

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3
Q

Example: Phosphate Buffer System

A
  • Buffer fixed acids within you body

pKa= 6.8

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4
Q

Two Kinds of Acid in Body: “Volatile” and “Fixed”

A

1) VOLATILE ACID: Carbonic Acid —> H2CO3
- In Chemical Equilibrium with CO2, a Volatile Gase:
H2CO3 CO2 + H2O

  • Pulmonary Ventilation controls H2CO3 Concentration in Body Fluids

2) FIXED ACIDS: Non Carbonic Acids generated Metabolically (Ex: Sulfuric, Phosphoric Acids)
- Initially Neutralized by Buffers in Body Fluids

  • Ultimately Excreted in Urine
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5
Q

Metabolic Sources of H+

A

1) OXIDATIVE METABOLISM: Co2 (15,000 mEq/ Day)
CO2 + H2O H2CO3 H+ + HCO3-

2) NONVOLATIEL (Fixed) ACIDS: 40 - 80 mEq/ day
- Glycolysis: Lactic Acid (pKa 3.9)

  • Incomplete Oxidation of Fatty Acids: Ketone Acid (pKa 4.5)
  • Protein, Nucleic Acid, Phospholipid Metabolism: Sulfuric, Phosphoric, Hydrochloric Acids
  • CANNTO BE REMOVED FROM BODY BY VENTILATION!!!!!!!!!
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6
Q

3 Lines of Defense against pH Changes

A

1) Chemical Buffers
2) Respiration
3) Kidneys

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7
Q

First Line of Defense: Chemical Buffers

A
  • Bicarbonate
  • Intracellular Fluid
  • Bone
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8
Q

Bicarbonate System is the Major EC BUFFER

A
  • Equilibrium between H2CO3 and HCO3 (pKa = 3.8)

pH = 3.8 log [HCO3-]/ [H2CO3]

  • H2CO3 is also in Equilibrium with CO2 and H2); CO2 Concentration is 400x [H2CO3]
  • CO2 Concentration is related to PCO2. For each mmHg PCO2, 0.3 millimolar CO2 is in Solution at 37 Degrees Celsius. Thus

pH = 6.1 + log [HCO3-]/ (0.03 x PCO2)

**Advantage: [HCO3-] and PCO2 are EASILY MEASURED!!!

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9
Q

Why is a Bicarbonate Buffer System so Powerful?

A
  • Components (HCO3-, CO2) are ABUNDANT
  • Bicarbonate Buffer System is “OPEN”; Concentration of HCO3- and CO2 are readily adjusted by Respiration and Renal Function

**RESPIRATORY adjustment HAPPENS FIRST!!!!!

**Kidneys CAN compensate for Lungs but Lungs CANT compensate for Kidneys!!!

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10
Q

Response of Bicarbonate System to Strong Acid

A

CLOSED SYSTEM:
- The [CO2] will build up and the pH will start to drop to around 6.2

OPEN SYSTEM:
- The [CO2] will be low and the pH will rise back to Normal

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11
Q

Renal Regulation of pH

A

Urine pH Range: 4.5 - 8.0!!!!!!!**

1) Renal Response to Excess ACID:
- All of filtered HCO3- is REABSORBED

  • Additional H+ is Secreted into Lumen, Excreted PRIMARILY as AMMONIUM (NH4+)!!!!!!!!!!!!!!

2) Renal Response to Excess BASE:
- Incomplete Reabsorption of filtered HCO3- (Secreted)

  • Decreased H+ Secretion
  • Secretion of HCO3- in COLLECTING DUCT
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12
Q

Renal Regulation of pH Stats

A
  • Each day, 40-80 mEq H+ are EXCRETED in URINE
  • Free Urinary [H+} is only 40 microbial/L at a pH of 4.5, thus daily Urine Volume of 2500L would be required to Excrete 100 mEq of H+ …. this is NOT PHYSIOLOGICALLY POSSIBLE
  • Most H+ is EXCRETED in combination with Urinary Biuffers. Two types:
    1) TITRATABLE ACID: Conjugate bases of Metabolic Acids (Phosphate, Creatinine, Urate) accept H+ in LUMEN

2) AMMONIA: Generated by Tubular Epithelium

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13
Q

Total Renal H+ Excretion

A
  • H+ Excretion = Urinaruy Excretion of Titratable Acid + Ammonium - HCO3
  • Typical Rates (mEq/day):
    24 + 48 - 2 = 70 mEq/ day

Note: HCO3 EXCRETION is Equivalent to ADDING Acid to Body Fluids (for each mEq of HCO3 lost, a free H+ is left behind)

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14
Q

Luminal pH along Nephron

A
  • Acidification of Luminal Fluid is rather modest (pH 6.7) before COLLECTING DUCT.
  • In Collecting Duct, Fluid can be Acidified to a pH as low as 4.5!!!!!!!!

**AMMONIA is FORMED in the PROXIMAL TUBULE

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15
Q

Collecting Ducts can Secrete H+ or HCO3-

A

1) ALPHA Intercalated Cells:
- ACTIVELY SECRETE H+

  • H+-ATPase
  • Up to 900 fold [H+] Gradient

2) Beta- Intercalated Cells
- Secrete HCO3 to Eliminate Excess base

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16
Q

Acid-Secreting Type A Intercalated Cells

A
  • Aldosterone INCREASES the activity of the ATPase and causes the ALPHA intercalated cells to EXCRETE H+ ions
17
Q

Acidification of Urine begins in Proximal Tubule

A
  • Most of the H+ Secreted by the PROXIMAL TUBULE is used to REABSORB Filtered HCO3-, so LUMINAL pH FALLS only SLIGHTLY (6.7) in this Segment
18
Q

Tubular Reabsorption of Filtered HCO3-

A
  • At 25 mEq/L Plasma concentration, 4500 mEq of HCO3- are filtered into Nephrons Per Day
  • EXCRETION of HCO3- has same effects as Gaining H+; EXCRETION of even Small Fraction of filtered HCO3- must be RECAPTURED
  • If Arterial pH is TOO HIGH, Kidneys respond by INCOMPLETELY REABSORBING HCO3-
19
Q

Mechanism to reabsorb Filtered HCO3-

A
  • CO2 is brought back into the Cell
  • CO2 combines to H2O in the cell to form H2CO3
  • H2CO3 dissociates into H+ and HCO3-
  • The HCO3- is REABSORBED back into the Blood
20
Q

Important Features of HCO3- Reabsorption

A
  • HCO3- is temporarily converted to CO2
  • Ultimately dependent on Na+, K+, ATPase
  • Process DOES NOT result in Secretion of H+***
  • By this Mechanism, about 80% of filtered HCO3- is Reabsorbed is PROXIMAL TUBULE, most of remainder in THICK ASCENDING LIMB
  • A SATURABLE Process: at [HCO3-] > 26 mEq/L, some is EXCRETED in URINE!!!
21
Q

Saturation of HCO3- Reabsorption

A
  • Once the HCO3- Transporters are Saturated, the Reabsorbed HCO3- starts to Plateau and the Excreted starts to Increase!!!
22
Q

Excretion of H+ as Titratable Acid

A
  • Filtered HPO4 2- is the MOST IMPORTANT BUFFER converted to TITRATABLE ACID
  • These buffers can bind to the H+ and Excrete them out!!!!!!!! (Titratable Acid)
23
Q

Excretion of H+ and AMMONIUM

A
  • Two NH4+ are generated by GLUTAMINE OXIDATION within the Tubular Epithelial Cells
  • Two HCO3- are produced by GLUTAMINE OXIDATION

We get an ACIDIFICATION of the Urine!!!!!***

24
Q

Chronic Acidemia (Elevated H+ Concentration) up-regulates Renal NH4+ Production, Excretion

A
  • Chronic Acidemia causes the URINARY AMMONIUM EXCRETION to Increase at a HIGHER RATE than it would under normal conditions
25
Q

Alkalemia (Reduction in H+ Concentration, Collecting Ducts Secrete HCO3-

A
  • Beta Intercalated Cells can Secrete HCO3- in the Collecting Duct!!!!!!!
26
Q

Factors Controlling Renal H+ Secretion

A

1) Intracellular pH:
- Ex: Decreased Intracellular pH causes H+ to be SECRETED

2) Plasma PCO2:
- Increased PCO2 caused H+ to be SECRETED

3) Carbonic Anhydrase Activity (Affecting H+ and HCO3-):
- We

4) Na+ Reabsorption (ECF Volume Changes due to Angiotensin/ Aldosterone):
- Ex: Increased Sodium Reabsorption causes for the H+ to be Secreted!!!

  • Look at the Body Volume Status

5) Extracellular [K+]:
- Ex: Decreased [K+] causes for the K= to be Reabsorbed and for the H+ to go into the cell which causes the H+ to be SECRETED leading to an ALKALOSIS

6) Aldosterone:
- Na Reabsorbed
- K Secreted
- H Secreted

27
Q

Diuretic Abuse can cause Alkalemia

A 
Volume Contracts (Dehydration) = HYPOKALEMIA
- The INCREASE in Distal Delivery of Na causes K= to be dumped out into the Lumen and be SECRETED!!!

Generated METABOLIC ALKALOSIS!!!!!!**

28
Q

Simple Acid-Base Disorders

A
  • Normal Arterial Plasma pH Range: 7.35 - 7.45
  • ACIDEMIA: A reduction in Arterial pH below 7.35
  • ACIDOSIS: Any abnormal condition that PRODUCES ACADEMIA
  • ALKALEMIA: An Increase in Arterial pH above 7.45
  • ALKALOSIS: Any Abnormal condition that PRODUCES ALKALEMIA
29
Q

Respiratory Acid-Base Distrurbances

A

1) RESPIRATORUY ACIDOSIS: Increased Arterial PCO2:
- Renal Response: INCREASED H+ Secretion RESTORES Extracellular pH, INCREASES HCO3- further
2) RESPIRATORY ALKALOSIS: Decreased Arterial PCO2:
- Renal Response: LESS H+ SECRETION, more HCO3- EXCRETION in Urine

30
Q

Metabolic Acidosis

A

Low Plasma pH (Lowered Ratio of HCO3- to PCO2) due to:
a) Gain of Fixed Acid in Body Fluids (Ketone Bodies, Lactic Acid) or

b) Loss fo HCO3- (Diarrhea)
- In either case, [HCO3-] FALLS!!!!!!!!

RESPIRATORY COMPENSATION: Increased VENTILATION (Peripheral Chemoreceptors)

RENAL COMPENSATION: Increased H+ Secretion; Production of new HCO3-
HCO3- formed in the Proximal Tubule

31
Q

Metabolic Alkalosis

A

Abnormally HIGH Plasma pH (Increased Ratio of HCO3- to PCO2) due to:
a) Excessive Gain of STRONG BASE or HCO3- (Alkali Ingestion)

b) Excessive Loss of Fixed Acid (Loss of GASTRIC ACID through Vomiting)
- HCO3- Concentration rises due to Shift in Carbonic Anhydrase Equilibrium toward HCO3-

RESPIRATORY COMPENSATION: Decreased VENTILATION

RENAL COMPENSATION:
- Incomplete Reabsorption of filtered HCO3-

  • Beta Intercalated Cells SECRETE HCO3-
32
Q

Primary Acid-Base Disturbances

A

1) Respiratory Alkalosis:
- pH INCREASES (Decr CO2) so HCO3- DECREASES

2) Respiratory Acidosis:
- pH DECREASES (Incr CO2) so HCO3- INCREASES

3) Metabolic Alkalosis:
- pH INCREASES (Incr HCO3) so CO2 INCREASES

4) Metabolic Acidosis:
- pH DECREASES (Decr HCO3) so CO2 DECREASES

***Compensation is NEVER COMPLETE

33
Q

Know Davenport Diagrams

A
  • Move Horizontally on the line for any type of RESPIRATORY CHANGE
  • Move Vertically on the line for any type of METABOLIC CHANGE
34
Q

Anion Gap

A
  • Used in Differential Diagnosis of Metabolic Acidosis
  • ****AG= Measured Cation (Na+) - Measured Anions (CL-, HCO3-)
  • Gap is comprised of UNMEASURED Anions including Plasma Albumin, Phosphate, Sulfate, Citrate, Lactate, Ketoacids
  • Normal Range: 8 - 16 mEq/L (Method Dependent)
  • Anion Gap is either NORMAL or INCREASED, depending on cause of Metabolic Acidosis

1) HYPERCHLORIC ACIDOSIS: AG is UNCHANGED
- Loss of HCO3- is matched by GAIN of CL-

2) HIGH ANION GAP ACIDOSIS (Normochloremic):
- HCO3- is replaced by UNMEASURED ANION (Lactate, Ketoacidosis, Poisoning)
- ——–> In this case the Anion Gap INCREASES!!!!

35
Q

Causes of High Anion Gap Acidosis

A

M- Methanol
U- Urea
D- Diabetic Ketoacidosis

P- Paraldehyde
I- Isonazide
L- Lactic Acid
E- Ethylene Glycol, Ethanol
S- Salicylic Acid (Aspirin)

Renal I (14 decks)

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