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Flashcards in Acid Base Balance Deck (32)
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1
Q

What pH indicates alkalemia and acidemia?

A

Alkalemia: >7.42
Acidemia: <7.38

2
Q

What is one danger of having an alkaline plasma?

A

since calcium is only soluble in acidic solutions, hypocalcemia can result in abnormal muscle firings producing twitches and tetany

3
Q

What can happen to the heart in acidemia?

A

Acidic conditions means there is an increase in H+ which will want to enter the cell. The only way to move H+ into the cell is to transport K+ out, and increasing K+ means pacemaker cells will repolarise too quickly = causing an arrhythmia

4
Q

What does plasma pH depend on? Which 2 organs are responsible for maintaining this balance?

A

The ratio of [HCO3-] to dissolved CO2, the ratio should be 20:1. This ratio is controlled by the lungs and the kidneys

5
Q

What can the kidneys compensate and correct for?

What can ventilation compensate and correct for?

A

Kidneys compensate for a respiratory pH imbalance and correct for a metabolic pH imbalance

Ventilation will compensate for a metabolic pH imbalance and correct for a ventilation pH imbalance

6
Q

How does metabolic acidosis occur? How does the body compensate AND correct for this?

A
  1. Tissues produce acid metabolically, which enters the blood and dissociates into H+ and an anion
  2. H+ reacts with HCO3- in the capillaries to produce CO2 and water
  3. CO2 travels back to the lungs and is lost

Therefore, for every mole of H+, you lose one mole of HCO3- and the net effect is acidic. The body has 2 options…
Correct: kidneys will reabsorb/make more HCO3-
Compensate: Ventilation increases to eliminate more CO2

7
Q

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

A

HCO3- is produced as a byproduct of creating acid in the stomach and immediately travels into the bloodstream. Normally it can recombine with H+ in the duodenum and neutralize, BUT if you’re vomiting up H+ it never makes it to the duodenum and there’s nothing to neutralize the HCO3- in the blood

Can only partially compensate as you can’t decrease ventilation without putting the patient at risk of hypoxia

8
Q

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

A
  1. In the PCT the kidneys can metabolize amino acids (N containing compounds):
    Glutamine gets broken down to produce alpha-ketoglutarate which makes HCO3- and NH4 (ammonia), ammonia reacts with H+ to make ammonium and neutralize the pee
  2. Na combines with HCO3- in the filtrate, NaHCO3- dissociates into Na and HCO3- :
    The HCO3- combines with H+ in the filtrate to form H20 and CO2, which diffuses across the luminal membrane and reforms H+ and HCO3-

The Na+ enters the Na/H+ exchanger and is resorbed into the cell and helps drive H+ movement into the filtrate

9
Q

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

A

Since the kidneys are highly metabolic they produce large quantities of CO2: CO2 reacts with water to produce

  1. HCO3- enters the plasma
  2. H+ which goes into the urine via 2 pumps: the H+ ATPase and the H+-K+ exchanger which uses K+ excreted by the principal cells via ROMK

Once in the filtrate H+ binds with phosphate or ammonia and is excreted

10
Q

Where is HCO3- recovered in the nephron?

A

80-90% is recovered in the PCT and the rest in the LOH

11
Q

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

A

It must be replaced by another anion, so acids that are produced metabolically dissociate into an H+ and an anion; e.g; ketones, lactate, etc

12
Q

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

A
  1. enhanced Na/H exchange so more HCO3- gets recovered from the filtrate in the PCT and LOH
  2. Enhanced ammonium production in the PCT
  3. Increased activity of H+ ATPase in DCT
13
Q

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

A

Because most HCO3 has been reabsorbed by the time it reaches the DCT so there’s no dissociation of NaHCO3- into Na and HCO3-. Therefore Na cannot be used in the sodium hydrogen exchanger and the H+ cannot be exported to the lumen, therefore you need active secretion of H+ ions

14
Q

What does the anion gap account for?

A

Determines whether HCO3- has been replaced by an anion other than Cl- by measuring the difference between anions and cations: [Na+] + [K+] – [Cl-] + [HCO3-]

15
Q

What does it mean if the anion gap is high? Name 3 examples of when this could occur and explain one in detail

A

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

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

Lactic acidosis: H+ and the anion lactate increase in the plasma, excess H+ is buffered by HCO3- to form CO2 and H2O - lowering the HCO3- levels in the plasma: SO there’s more lactate and less HCO3-

16
Q

What is meant by a normal anion gap?

A

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

17
Q

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?

A

A high anion gap and low HCO3-: means there’s been acid produced metabolically

If HCO3- is low and there’s a normal anion gap: A normal anion gap indicates there’s no high amounts of metabolic anions, but since HCO3- is STILL low it could mean there’s a renal problem that the kidney has compensated for with Cl-.

18
Q

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

That being said, how should you rebalance the pH of a patient who is excessively vomiting?

A

Normally a rise in intracellular pH means the kidney would secrete more HCO3- and preserve more H+, BUT when someone is excessively vomiting the patient becomes dehydrated and the kidney is preoccupied with retaining solutes and water and is less able to excrete the excessive HCO3-.

In order to treat the patient, you must rehydrate them so the kidney is able to focus on excreting more HCO3-.

19
Q

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

A

Extracellular: 3.5-5 mmol/L

Intracellular: 130 mmol/L

20
Q

What is the danger of hypokalemia?

A

Not enough K+ prolongs the AP/QT interval in pacemaker cells, this can trigger an after depolarisation and cause an arrhythmia; bradycardia

21
Q

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

A
  1. Ingestion of K+, as 90% of ingested K+ gets resorbed
  2. K+ loss through the body occurs in the kidneys which is relatively slow, and some K+ is lost in the gut (which increases when you vomit or have diarrhea)
22
Q

How is ECF [K+] controlled short term?

A

K+ is quickly moved in and out of cells via different pumps and with the help of insulin

23
Q

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

A
  1. Na+/K+ ATPase pump moves K+ into the cell and na+ out to maintain membrane potential
  2. K+ can leave the cell through the K+/H+ exchanger: when plasma is acidic more H+ enters the cell and is exchanged for K+ and a rise in plasma [K+] means more H+ is exported from the cell and K+ brought in

K+ can also leak out of cells or move out of excitable cells during APs

24
Q

Where in the nephron is K+ resorbed?

A

The PCT, LOH and DCT

25
Q

What 3 things can stimulate K+ excretion?

A

K+ movement into the lumen is stimulated by:

  1. High ECF [K+]
  2. Aldosterone: by increasing Na+ resorption (Na+/K+ ATPase)
  3. High ECF pH: Body should be excreting more K+ so more H+ is retained
26
Q

At which part of the DCT is K+ resorbed?

How does the ECF pH influence this resorption?

A

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

This is driven by the pH of the ECF:

  1. A low ECF pH will mean more H+ is excreted and K+ resorbed
  2. A high ECF pH will mean more K+ is excreted and more H+ retained
27
Q

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

A

Acidic pH: means more K+ is excreted and can lead to hyperkalemia

Alkaline pH: less K+ resorbed which can lead to hypokalemia

28
Q

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

A

K+ is absorbed and insulin secreted, moving K+ rapidly into cells preventing hyperkalemia.

Some H+ is excreted via H+/K+ exchanger, but since there’s now extra HCO3- in the blood coming from the stomach (as more acid is synthesized to breakdown the food) it neutralizes the H+.

29
Q

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

A

Lactic acidosis means H+ will move into cells and K+ into the plasma. Although the ECF [K+] tends to rise, other mechanisms are rapidly excreting H+ from the body, such as:
1. Respiration increases: which lowers pCO2 and H+
2. Kidney exports more H+
(and H+ is neutralized by HCO3- in the plasma)

So soon after, K+ is able to go back into the cells and hyperkalemia doesn’t occur

30
Q

How does the body avoid hypokalemia when someone is excessively vomiting or has diarrhea? How should you treat this?

A

The ECF [HCO3-] increases and [H+] falls, so more K+ moves into the cells.

BUT the kidney is also trying to compensate for dehydration by retaining more H+ so it should never fully drop, (and plasma [K+] shouldn’t drop)

Usually correcting the dehydration will sort it all out

31
Q

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

A
  1. No insulin in the body means the cells produce ketones and less K+ enters cells
  2. The ECF [H+] is also rising (due to ketones), so more H+ will enter the cells and K+ will leave

BUT the ECF [K+] never rises as the kidneys will lose the extra electrolytes in the urine along with extra water that followed the solutes

32
Q

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

A

If you give insulin:

Pro: Move more K+ back into the cells and ketone production will reduce

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