Xx - Renal Physiology Vi

Front 1

Volatile acid example(s)

How are these Acids formed?

Back 1

CO2

Cellular AEROBIC metabolism

Front 2

Nonvolatile acid example(s)

How are these acids formed?

Back 2

1.) Sulfuric acid
(Protein catabolism)

2.) Phosphoric acid
(Phospholipid catabolism)

Front 3

Which acid is AKA a "Fixed Acid?"

What is the "Fixed" amount?

Back 3

Nonvolatile Acid

Produced at 40 to 60 mmol/day

Front 4

What other Fixed acids are overproduced during diseased states

Back 4

Lactic Acid
Ketoacids
Salicylic acid

Front 5

Buffers most effective when?

What is this called on a Titration curve?

Back 5

pH is within 1 pH unit of pK

Linear portion

Front 6

Major EXTRACELLULAR BUFFER is?

Produced how?

Where?

Back 6

Bicarb (HCO3-)

CO2 + H2O <==> H2CO3 <==> H+ + HCO3-
(via Carbonic Anhydrase)

Alpha-Intercalated Cells

Front 7

Major URINARY BUFFER is?
(also a minor extracellular buffer)

This Urinary Buffer is AKA?

Back 7

Phosphate = (HPO4)2-

Titratable Acid

Front 8

pK of CO2/HCO3- buffer pair?

Back 8

6.1

Front 9

pK of (H2PO4)1- / (HPO4)2- buffer pair?

Back 9

6.8

Front 10

2 Categories of INTRACELLULAR BUFFERS

Back 10

Organic Phosphates
(AMP, ADP, ATP, 2,3-DPG, ...etc)

Proteins

Front 11

Specifically name the Major INTRACELLULAR BUFFER.

Back 11

Hemoglobin

Front 12

Which is a better intracellular buffer, Deoxyhemoglobin or Oxyhemoglobin?

Back 12

Deoxyhemoglobin

Front 13

Henderson Hasselbalch Eq.

Back 13

pH = pK + log ([A-]/[HA])

Front 14

For the HH equation, when would pH equal the pK?

Back 14

[A-] = [HA]

Front 15

BICARB REABSORPTION

- occurs primarily where?

- what transporter is used?

Back 15

Early PT

Na+/H+ Countertransporter

Front 16

BICARB REABSORPTION

- accounts for NET what?

- but does NOT account for Net what?

Back 16

Net Bicarb Resorption

Net H+ Secretion

Front 17

BICARB REABSORPTION

- under what conditions would Bicarb be excreted?

- give example of a clinical condition where this occurs

Back 17

- Filtered Load exceeds Resorptive Capacity due to Plasma[Bicarb] levels being too high

- Metabolic Alkalosis

Front 18

BICARB REABSORPTION

- Increased PCO2 effects?

- Decreased PCO2 effects?

Back 18

- Increased Bicarb Reabsorption

- Decreased Bicarb Reabsorption

Front 19

BICARB REABSORPTION

- ECF Expansion effects?

- ECF Contraction effects?

Back 19

- Decreased Bicarb reabsorption

- Increased Bicarb reabsorption

Front 20

BICARB REABSORPTION

- Angiotensin II effects?

Back 20

Increases Bicarb reabsorption

Front 21

BICARB REABSORPTION

- what leads to secondary CONTRACTION ALKALOSIS?

- what hormone Contributes additionally to the Contraction Alkalosis?

- what drugs can also lead to Contraction alkalosis?

Back 21

- ECF Contraction

- Angiotensin II

- Loops
- Thiazides

Front 22

FIXED H+ EXCRETION

- Fixed H+ is produced from what type of metabolism

- Fixed H+ is secreted into the TF from where?

Back 22

Protein catabolism
Phospholipid catabolism

Alpha-Intercalated cells of DT/CD

Front 23

FIXED H+ EXCRETION

- Fixed H+ is excreted in what 2 forms?

Back 23

Titratable acid (H2PO4)1-

NH4+

Front 24

FIXED H+ EXCRETION

- Fixed H+ is secreted into the urinary lumen from what cells?

- what transporter is used?

- in the urine, the H+ will join with what buffer?

Back 24

Alpha-Intercalated Cells

H+ ATPase

1.) (HPO4)2-
2.) NH3+

Front 25

FIXED H+ EXCRETION

- within the a-intercalated cell, the H+ dissociates from what?

- where does the dissociated thing go?

Back 25

- Bicarb ("Newly synthesized HCO3-)

- Reabsorbed into blood

Front 26

FIXED H+ EXCRETION

- the H+ secreted from the a-intercalated cell accounts for what?

- the Bicarb resorption from the a-intercalated cell accounts for what?

Back 26

- Net Secretion of H+

- Net Reabsorption of "Newly synthesized" Bicarb
(into the blood)

Front 27

FIXED H+ EXCRETION

- The H+ ATPase is found on what cell?

- What hormone increases the activity of the H+ ATPase?

Back 27

Alpha-intercalated cells of the DT/CD

Aldosterone

Front 28

FIXED H+ EXCRETION

- Excretion of Fixed H+ as a Titratable acid is dependent on what 2 things?

Back 28

- Amount of Urinary Buffer (HPO4-)

- Buffer pK

Front 29

FIXED H+ EXCRETION

- what is the minimum urinary pH occuring from excretion of Fixed H+ as Titratable acid?

Back 29

pH = 4.4

Front 30

FIXED H+ EXCRETION

- Excretion of Fixed H+ as NH4+ is dependent on what 2 things?

Back 30

Amount of NH3 synthesized

Urine pH

Front 31

FIXED H+ EXCRETION

- the NH3 used in urinary buffers is produced in what cells?

- the NH3 is made from what?

Back 31

Renal cells

Glutamine

Front 32

FIXED H+ EXCRETION

- as the urine becomes more acidic, DIFFUSION TRAPPING is what?

Back 32

Excretion of (basic) NH4+ in an Acidic Urine

(a base in an acid is "trapped")

Front 33

FIXED H+ EXCRETION

- an ADAPTIVE Increase in NH3 Synthesis occurs when?

Back 33

ACIDOSIS

Front 34

FIXED H+ EXCRETION

- What electrolyte condition INHIBITS NH3 synthesis?

Back 34

Hyperkalemia

(thus decreasing H+ excretion in NH4+ form)

Front 35

FIXED H+ EXCRETION

- What electrolyte condition STIMULATES NH3 synthesis

Back 35

HYPOKalemia

(thus increasing H+ excretion in NH4+ form)

Front 36

RENAL TUBULAR ACIDOSIS IV

- what type of acidosis is RTA 4?

- as a result, what happens to the H+ excretion?

Back 36

Hyperkalemic Hyperchloremic acidosis

Decrease in H+ excretion as NH4+

Front 37

METABOLIC ACIDOSIS

- pH
- [Bicarb] serum
- pCO2

Back 37

- Decrease
- Decrease
- Decrease

Front 38

METABOLIC ALKALOSIS

- pH
- [Bicarb] serum
- pCO2

Back 38

- Increase
- Increase
- Increase

Front 39

RESPIRATORY ACIDOSIS

- pH
- [Bicarb] serum
- pCO2

Back 39

- Decrease
- Increase
- Increase

Front 40

RESPIRATORY ALKALOSIS

- pH
- [Bicarb] serum
- pCO2

Back 40

- Increase
- Decrease
- Decrease

Front 41

METABOLIC ACIDOSIS

- due to?

- primary disturbance?

- compensation?

Back 41

Increased Arterial [H+] due to:
-Fixed Acid Overproduction/Ingestion
OR
-Base Loss

- Decreased Bicarb

- Hyperventilation (decreases PCO2)

Front 42

METABOLIC ALKALOSIS

- due to?

- primary disturbance?

- compensation?

Back 42

Decreased Arterial [H+]

- Increased Bicarb

- Hypoventilation (Increased CO2)

Front 43

RESPIRATORY ACIDOSIS

- due to?

- primary disturbance?

- compensation?

Back 43

1.) Decreased Respiratory Rate
2.) CO2 Retention

- Increased PCO2

- Increased H+ Excretion
- Increased Bicarb Reabsorption

Front 44

RESPIRATORY ALKALOSIS

- due to?

- primary disturbance?

- compensation?

Back 44

1.) Increased Respiratory Rate
2.) CO2 Loss

- Decreased PCO2

- Decreased H+ Excretion
- Decreased Bicarb Reabsorption

Front 45

Serum Anion Gap

- in what acid/base disorder?

- represents?

Back 45

- Metabolic Acidosis

- Unmeasured Anions

Front 46

Serum Anion Gap

- Equation?

- Normal value of AG?

Back 46

[Na+] - ( [Bicarb] + [Cl-] )

Nml = 12 mEq/L (+/- 4 mEq/L)

Front 47

Serum Anion Gap

- Increased serum AG implies what in Metabolic Acidosis?

Back 47

- Unmeasured Anions have Increased and Replaced the Loss of Bicarb

Front 48

Serum Anion Gap

- Normal serum AG implies what in Metabolic Acidosis?

Back 48

- [Cl-] increased and Replaced the Loss of Bicarb

Front 49

Serum Anion Gap

- Metabolic Acidosis with a NORMAL AG is also called what?

- Give clinical examples

Back 49

Hyperchloremic Metabolic Acidosis

- Diarrhea
- RTA I, II, IV

Front 50

Increased Bicarb reabsorption
AND
Activation of RAAS

- occurs in what specific acid/base disorder?

- Clinical condition example?

- Drugs that can induce this?

Back 50

Metabolic Alkalosis + ECF volume Contraction
(contraction alkalosis)

- Vomiting

- Loops & Thiazide diuretics

Front 51

Increased pCO2 is the primary disturbance for?

Increased pCO2 effects on serum levels?

MOA?

Back 51

Respiratory Acidosis

- Increased [H+]
- Increased [Bicarb]

Mass Action

Front 52

Decreased pCO2 is the primary disturbance for?

Decreased pCO2 effects on serum levels?

MOA?

Back 52

Respiratory Alkalosis

- Decreased [H+]
- Decreased [Bicarb]

Mass Action