Acid Base balance Flashcards
What pH indicates alkalemia and acidemia?
Alkalemia: >7.42Acidemia: <7.38
What is one danger of having an alkaline plasma?
Calcium only soluble in acidic solutions
*hypocalcemia -> abnormal muscle firings = twitches and tetany
What can happen to the heart in acidemia?
Acidic conditions means high ECF [H+] -> wants to enter cell
Only channel is H/K antiport - hyperkalemia means pacemakers repolarize too quickly = arrhythmia
What does plasma pH depend on and which organs are responsible for this?
Ratio of [HCO3-] to dissolved CO2 (should be 20:1)
Controlled by lungs and kidneys
What can the kidneys compensate and correct for? What can ventilation compensate and correct for?
Kidneys compensate for respiratory pH imbalance and correct metabolic pH imbalance
Ventilation compensates for metabolic pH imbalance and corrects ventilation pH imbalance
How does metabolic acidosis occur?
How does the body compensate AND correct for this?
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
How does metabolic alkalosis occur? How can you partially compensate for this?
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
How do the kidneys replace lost HCO3- in the PCT? List both ways
- 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
- 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
How do the kidneys replace lost HCO3- in the alpha intercalated cells of the DCT?
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
Where is HCO3- recovered in the nephron?
PCT: 80-90%
Rest: LOH
What must the body do in general to compensate for lost HCO3-?
Replaced w another anion
So metabolically produced acids dissociate into H+ and an anion, i.e ketones, lactate, etc
In summary, give 3 cellular responses in the kidney to acidosis
Enhanced..
1. Na/H exchange (recovers more HCO3) in PCT and LOH
- Ammonium production in PCT
- H+ ATPase activity in DCT
Why can’t excretion of H+ from the DCT use the Na gradient like the rest of the nephron?
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
What does the anion gap account for?
Determines whether HCO3- has been replaced by an anion other than Cl
by measuring the difference between anions and cations: [Na+] + [K+] – [Cl-] + [HCO3-]
What does it mean if the anion gap is high? Name 3 examples of when this could occur
Means the unmeasured anions account for a greater proportion of the serum’s (-) charge than usual
E.g; lactic acidosis, diabetic ketoacidosis, methanol poisoning
What is meant by a normal anion gap?
Means patient’s HCO3-, Cl-, Na+ and K+ levels are all normal
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 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-
Why is it hard for the kidney to correct high pH when someone is excessively vomiting?
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-
What is the normal range of extracellular and intracellular [K+]?
Extracellular: 3.5-5 mmol/LIntracellular: 130 mmol/L
What is the danger of hypokalemia?
Prolongs AP/QT interval -> arrhythmia; bradycardia
Name 2 medium-long term factors that affect the ECF [K+]
- Ingestion of K+ (90% resorbed)
2. K+ loss occurs in kidneys (relatively slow) and some gut (increases with vomiting or diarrhea)
Name 2 pumps that move K+ in and out of cells and how K+ can leave cells without a pump
- Na+/K+ ATPase
- K+/H+ exchanger
Leak out of excitable cells during APs
Where in the nephron is K+ resorbed?
The PCT, LOH and DCT
2 things that can stimulate K+ reabsorption
K+ movement into the lumen is stimulated by:
Low ECF pH, aldosterone
At which part of the DCT is K+ resorbed?
In the alpha intercalated cells K+ is reabsorbed in exchange for H+.
*influenced by ECF pH
What are the consequences of an acidic or alkaline pH in terms of [K+]?
Acidic pH -> hyperkalemia
Alkaline pH -> hypokalemia
Why doesn’t the body go into acidosis or hyperkalemia when K+ is ingested?
Insulin secreted: moves K+ into cells
Extra HCO3- (produced as byproduct of acid from stomach) neutralizes any H+ excreted via H/K exchanger
Why doesn’t the body go into hyperkalemia after lactic acidosis?
Respiration increases (lowers pCO2 and H+), kidney exports more H+, H+ neutralised with HCO3- in plasma
ignore
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What happens to the ECF [K+] in diabetic ketoacidosis?
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)
What are the pros and cons of giving insulin to treat diabetic ketoacidosis?
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
What stimulates the central vs peripheral chemoreceptors and where are they?
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
Explain how lactic acidosis results in a high anion gap?
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
