Acid Base balance

Question 1

What pH indicates alkalemia and acidemia?

Answer 1

Alkalemia: >7.42Acidemia: <7.38

Question 2

What is one danger of having an alkaline plasma?

Answer 2

Calcium only soluble in acidic solutions

*hypocalcemia -> abnormal muscle firings = twitches and tetany

Question 3

What can happen to the heart in acidemia?

Answer 3

Acidic conditions means high ECF [H+] -> wants to enter cell

Only channel is H/K antiport - hyperkalemia means pacemakers repolarize too quickly = arrhythmia

Question 4

What does plasma pH depend on and which organs are responsible for this?

Answer 4

Ratio of [HCO3-] to dissolved CO2 (should be 20:1)

Controlled by lungs and kidneys

Question 5

What can the kidneys compensate and correct for? What can ventilation compensate and correct for?

Answer 5

Kidneys compensate for respiratory pH imbalance and correct metabolic pH imbalance

Ventilation compensates for metabolic pH imbalance and corrects ventilation pH imbalance

Question 6

How does metabolic acidosis occur?

How does the body compensate AND correct for this?

Answer 6

Tissues produce lactic acid -> enters blood and dissociates into H+ and an anion

H+ and HCO3 = CO2 and water (CO2 is lost in lungs)

So for every mole of H+, you lose one mole HCO3 = net acidic effect

Kidneys CORRECT by reabsorbing more HCO3-
Lungs COMPENSATE by eliminating more CO2

Question 7

How does metabolic alkalosis occur? How can you partially compensate for this?

Answer 7

HCO3- is produced as a byproduct of creating acid in the stomach -> bloodstream and normally combines with H+ in DD to neutralize

VOMITING loses H+
= metabolic alkalosis

Partially compensate as can’t decrease ventilation without putting patient at risk of hypoxia

Question 8

How do the kidneys replace lost HCO3- in the PCT? List both ways

Answer 8

1. Metabolize amino acids: Glutamine breaks down to produce alpha-ketoglutarate which makes HCO3- and NH4 (ammonia), ammonia reacts with H+ to make ammonium and neutralizes pee
2. In filtrate: Na+ combines and dissociates from HCO3-> HCO3 and H+ -> H20 and CO2 -> diffuses across luminal membrane and reforms H+ and HCO3
   * Na/H+ exchanger on luminal membrane resorbs Na+ and pumps H+ into filtrate

Question 9

How do the kidneys replace lost HCO3- in the alpha intercalated cells of the DCT?

Answer 9

Kidney cells highly metabolic: produce lots of CO2

CO2 + H20 ->
HCO3: enters plasma
H+: Enters filtrate via H+ ATPase and H/K exchanger which uses K+ excreted via ROMK in the principal cells
-> binds with phosphate or ammonia -> excreted

Question 10

Where is HCO3- recovered in the nephron?

Answer 10

PCT: 80-90%
Rest: LOH

Question 11

What must the body do in general to compensate for lost HCO3-?

Answer 11

Replaced w another anion

So metabolically produced acids dissociate into H+ and an anion, i.e ketones, lactate, etc

Question 12

In summary, give 3 cellular responses in the kidney to acidosis

Answer 12

Enhanced..
1. Na/H exchange (recovers more HCO3) in PCT and LOH

2. Ammonium production in PCT
3. H+ ATPase activity in DCT

Question 13

Why can’t excretion of H+ from the DCT use the Na gradient like the rest of the nephron?

Answer 13

Most HCO3 has been reabsorbed by the time it reaches the DCT = no NaHCO3 dissociation and N/H channel

Need active secretion of H+ ions

Question 14

What does the anion gap account for?

Answer 14

Determines whether HCO3- has been replaced by an anion other than Cl

by measuring the difference between anions and cations: [Na+] + [K+] – [Cl-] + [HCO3-]

Question 15

What does it mean if the anion gap is high? Name 3 examples of when this could occur

Answer 15

Means the unmeasured anions account for a greater proportion of the serum’s (-) charge than usual

E.g; lactic acidosis, diabetic ketoacidosis, methanol poisoning

Question 16

What is meant by a normal anion gap?

Answer 16

Means patient’s HCO3-, Cl-, Na+ and K+ levels are all normal

Question 17

What could it mean if there’s low HCO3- and an increased anion gap?

What does it mean if there’s low HCO3- and a normal anion gap?

Answer 17

A high anion gap and low HCO3-: means acid produced metabolically (i.e lactic acid)

Gap normal bu HCO3- STILL low: renal problem that kidney has compensated for with Cl-

Question 18

Why is it hard for the kidney to correct high pH when someone is excessively vomiting?

Answer 18

Kidney preoccupied with retaining solutes/water and is less able to excrete excessive HCO3

*treat first with rehydration so kidney can focus on excreting HCO3-

Question 19

What is the normal range of extracellular and intracellular [K+]?

Answer 19

Extracellular: 3.5-5 mmol/LIntracellular: 130 mmol/L

Question 20

What is the danger of hypokalemia?

Answer 20

Prolongs AP/QT interval -> arrhythmia; bradycardia

Question 21

Name 2 medium-long term factors that affect the ECF [K+]

Answer 21

1. Ingestion of K+ (90% resorbed)

2. K+ loss occurs in kidneys (relatively slow) and some gut (increases with vomiting or diarrhea)

Question 22

Name 2 pumps that move K+ in and out of cells and how K+ can leave cells without a pump

Answer 22

1. Na+/K+ ATPase
2. K+/H+ exchanger

Leak out of excitable cells during APs

Question 23

Where in the nephron is K+ resorbed?

Answer 23

The PCT, LOH and DCT

Question 24

2 things that can stimulate K+ reabsorption

Answer 24

K+ movement into the lumen is stimulated by:

Low ECF pH, aldosterone

Question 25

At which part of the DCT is K+ resorbed?

Answer 25

In the alpha intercalated cells K+ is reabsorbed in exchange for H+.

*influenced by ECF pH

Question 26

What are the consequences of an acidic or alkaline pH in terms of [K+]?

Answer 26

Acidic pH -> hyperkalemia

Alkaline pH -> hypokalemia

Question 27

Why doesn’t the body go into acidosis or hyperkalemia when K+ is ingested?

Answer 27

Insulin secreted: moves K+ into cells

Extra HCO3- (produced as byproduct of acid from stomach) neutralizes any H+ excreted via H/K exchanger

Question 28

Why doesn’t the body go into hyperkalemia after lactic acidosis?

Answer 28

Respiration increases (lowers pCO2 and H+), kidney exports more H+, H+ neutralised with HCO3- in plasma

Question 29

ignore

Answer 29

ok

Question 30

What happens to the ECF [K+] in diabetic ketoacidosis?

Answer 30

No insulin: less K+ enters cells BUT body produces ketones (ECF [H+] rises)

ECF [K+] doesn’t rise as kidney loses extra electrolytes in urine
(along with water that followed solutes)

Question 31

What are the pros and cons of giving insulin to treat diabetic ketoacidosis?

Answer 31

Pro: Moves more K+ into the cells and reduces ketone production

Con: Since body has already excreted most of its K+, giving insulin may make the body go into hypokalemia

Question 32

What stimulates the central vs peripheral chemoreceptors and where are they?

Answer 32

Peripheral: Carotid and aortic bodies, stimulated by high pCO2, low pH and pO2

Central: pH and pCO2 changes of CSF
*less responsive with chronic increases in pCO2

Question 33

Explain how lactic acidosis results in a high anion gap?

Answer 33

H+ and the anion lactate increase in plasma, excess H+ buffered by HCO3- (forms H20 and CO2) -> lowering plasma HCO3-

SO there’s more lactate and less HCO3- = high anion gap