Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Renal > Acid-Base Disorders > Flashcards

Acid-Base Disorders Flashcards

1
Q

What are the 3 main ways the body produces acid?

A
  1. dietary intake:
    - lysine and arginine –> H+
    - cysteine and methionine –> sulfuric acid
    - proteins–> phosphoric acid
  2. incomplete metabolism of glucose –> lactic acid
  3. Stool HCO3
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the bodies main defense to maintain the extracellular pH?

A
  1. HCO3/CO2 buffer system

H+ and HCO3 -> H2CO3– carbonic annhydrase–> H20 + CO2

The lung blows off excess CO2 so the net result is a decrease in HCO3 and slight decrease in pH instead of LARGE decrease that would be expected without the buffer

  1. other buffer systems that utilize pH in ECF
  2. bone/cell buffers like Hb
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the major effect of buffering on total body acid?

A

Buffers decrease the effect of net acid addition on the pH of the ECF, however, they do NOT remove excess acid from the body.

The kidneys are necessary for removal of non-volatile acids/bases and the lungs are necessary for the removal of volatile acids/bases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is Henderson-Hasselbach equation?

A

pH = 6.1 + log [HCO3]/apCO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

An increase in pCO2 of the blood leads to a ______ in the blood pH and consequently is called ______________________.

A

decrease in the pH and is respiratory acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

A decrease in pCO2 of the blood leads to a _____________ in the blood pH and consequently is called___________________.

A

increase and is called respiratory alkalosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

A decrease in HCO3 concentration leads to a _____________in pH and is called______________.

An increase in HCO3 leads to a _____________in pH and is called ___________.

A

Decreased HCO3 lowers pH and is metabolic acidosis

Increased HCO3 leads to high pH and is metabolic alkalosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

If there are similar proportional changes to HCO3 and pC02, what will the effect be on pH?

A

If HCO3 goes from 24 to 12 and pCO2 goes from 40 to 20, there will be no effect on pH.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the effect of the endogenous production of metabolic acids on the plasma HCO3? How do the lungs responds?

A

Increase in production of endogenous acid decreases the HCO3 (metabolic acidosis)
The lungs respond by decreasing CO2 (breathing heavier to blow off acid)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the 2 major functions of the kidney in regard to HCO3?
Where does each action occur?

A
  1. Reclamation- they will recapture HCO3 that has been filtered in the proximal tubule
  2. Regeneration - occurs in collecting duct
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How does the proximal tubule reclaim HCO3?

A

When there is metabolic acidosis,

H+ is secreted from the cell into the lumen where it reacts with HCO3 to make H2CO3.

Carbonic annhydrase converts it to H20 and CO2 which freely diffuse into the cell
Carbonic anhydrase in the cell reforms H2CO3 that dissociates into H+ and HCO3-.

The HCO3- goes into the blood, and the H+ goes into the lumen to reclaim more

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the effect of EABV on the reclamation of HCO3 in the proximal tubule?

A

If there is low EABV, there will be increased reclamation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the effect of K on reclamation of HCO3?

A

If there is low K+, there will be enhanced reabsorption of HCO3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

If 70mEq of acid are added to the ECF, how many HCO3 molecules must be regenerated?

A

The kidney must reclaim all the filtered HCO3 and then regenerate 70 mEq of base .

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe the process of HCO3 regeneration in the collecting duct.

A

There are titratable buffers like phosphate and creatinine that are filtered through the glomerulus and are titrated by H+ to acid form.

Non-titratable buffers like NH3 are permeable across the collecting duct. H+ secretions convert NH3 to NH4 which is impermeable and gets trapped in the lumen .

Acidification of the lumen leads to NH3 trapping and pushes an HCO3 back into the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the 4 factors that regulate H+ secretion from intercalated cells in the CCD?

A
  1. blood pH
  2. mineralocorticoid level (aldo directly and indirectly) and distal delivery of Na
  3. K+ deficiency will excrete H+
  4. volume depletion increased H+ secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the effect of pH on the synthesis of ammonia in the proximal tubule?

A

Acidosis increases ammonia synthesis and alkalosis inhibits it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the equation for net acid excretion (NAE)?

A

NAE = Unh4V + UtaV - Uhco3V

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the 4 steps to analyzing electrolytes?

A
  1. Look at [Na] and if abnormal work up tonicity disorders (normal if 140)
    - if above 140 consider low H20 (hypernatremia)
    - if below 140 consider high H20 (hyponatremia)
  2. Check [Cl] and how it compares to [Na}. They should rise and fall together. (normal Cl =100)
    - if Cl rises with respect to Na, consider NG metabolic acidosis, chronic respiratory alkalosis
    - if Cl drops with respect to Na consider
    chronic respiratory acidosis, metabolic alkalosis
  3. Calculate the anion gap: Na- (HCO3 + Cl)
  4. If anion gap is increased, determine whether HCO3 is equal to predicted HCO3
  5. Analyze ABG
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

For acute respiratory acidosis, for every increase in 10mmHG pC02, what should be the rise of bicarb?

A

1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

For chronic respiratory acidosis, for every increase in 10mmHg CO2, what is the rise of bicarb?

A

3.5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

For acute respiratory alkalosis, for every fall of 10mmHg CO2, what is the change to HCO3?

A

2

23
Q

For chronic respiratory alkalosis, for every fall of 10mmHg CO2, what is the decrease of HCO3?

A

5

24
Q

How do acute compensations occur?

How do chronic compensation occur?

A

Acute- RBC exchange

Chronic - renal mechanisms

25
Q

For metabolic acidosis, how do you calculate appropriate compensations?

A

For each drop in HCO3, there should be a CO2 drop of 1.2

CO2 = HCO3 +15
CO2 = last digit of pH
26
Q

For metabolic alkalosis, how do you calculate appropriate compensation?

A

For each increase in HCO3, the CO2 should increase by 0.7

27
Q

How is the plasma anion gap calculated?
What is the normal anion gap?

What does an increased anion gap tell you?

A

[Na] - ([HCO3] +[Cl])

Normal anion gap is 8-16 (but usually 12-14mEq/L)

If the anion gap is increased, it marks the:

  1. presence/increase of an unmeasured anion (ex. hyperphosphatemia, increased valency of albumin)
  2. decrease of unmeasured cations (hypocalcemia, hypomagnesemia)
  3. generation of metabolic acidosis with a non-Cl acid
28
Q

What is the effect of a decrease of NaHCO3- to total body Cl, Na, HCO3, unmeasured anions?

A

It will decrease total body Na and HCO3.
There will be no increase in total body Cl and no change in unmeasured anions.

This leads to metabolic acidosis, volume depletion, and/or hypotonic state.

The body responds by inhibiting ADH because of the hyponatremia, and increasing retention of Na and Cl.

The ultimate result then is:
1. loss HCO3
2. no change in Na
3, increase in Cl
NO ANION GAP CHANGE
29
Q

What are the 5 classifications of NG metabolic acidosis?

A
  1. Dilutional acidosis
  2. Addition of HCl or Equivalent
  3. GI HCO3 loss
  4. RTA
  5. Addition of unmeasured anion that is excreted
30
Q

What is dilutional acidosis?

A

It is a normal gap metabolic acidosis that is due to administration of saline that dilutes plasma HCO3 concentrations.

31
Q

Describe how the addition of acid with an unmeasured anion that is excreted can cause NG metabolic acidosis.

A

A patient originally has an organic acid metabolic acidosis (anion gap).
The organic anion may be excreted before the metabolic acidosis is corrected.
DKA where they have good kidney function and are treated with saline. This clears out the ketoacid, and gives the appearance of a hyperchloremic acidosis.

32
Q

How can you tell if a patient has RTA vs. another kind of metabolic acidosis?

A

If there is an acidosis, the body should increase acid excretion to reduce the acidosis.
If it is RTA, there will be no increase in acid excretion.

33
Q

What are the 3 types of RTA?

A

Type1 - hypokalemic distal RTA, medullary collecting duct can’t acidify urine
Type 2- proximal RTA- proximal tubule can’t reclaim HCO3
Type 4- Hyperkalemic distal RTA- CCD cant secrete K or H

34
Q

How can the urinary acid secretion tell you if the acidosis is renal or extrarenal?

A

UAG = [Na]+[K]-[Cl] is a good surrogate for UNH4 and in order to figure out urinary acid secretion you use:
UNH4 V + UTA V - UHCO3 V

If urine pH < 6.5, HCO3 is less than 3
pH is a good surrogate for UTA

If there is increased renal acid secretion, it is extrarenal. (>30-60mEq/day

35
Q

Why is UAG negative if there is being acid secreted in the urine?

A

The Cl will increase making the UAG negative.
Cl increases because it is excreted as NH4Cl.
NH4 is made from NH3 in the lumen and H+ secreted by the kidney showing acid is being secreted .

36
Q

What are major conditions that cause increased anion gap?

A
  1. Lactic Acidosis (circ, collapse, anemia, hypoxemia, metabolic blockade, seizures)
  2. Ketoacidosis (diabetic, alcoholic, starving)
  3. Renal failure
  4. Overdoses (methanol, ethylene glycol, salicylates)
37
Q

What is the Cori cycle?

A
  1. Lactic acid is released into the blood and forms sodium lactate and consumes an HCO3.
  2. Liver removes Na lactate, converts it to lactic acid which gets converted to CO2 and H20 regenerating the HCO3
38
Q

What causes diabetic ketoacidosis?

What 3 substances are generated and which can be detected by nitroprusside test for ketone bodies?

A

In the absence of insulin, glucose cannot get into cells. The glucose then gets converted to:

  1. beta-hydroxybutyric acid
  2. acetoacetic acid - NP
  3. acetone -NP
39
Q

Why does CKD cause anion gap ketoacidosis?

A

RTA of Renal Insufficiency and Uremic acidosis are caused by the failure of tubular acidification process to excrete the normal daily acid loads.

  1. In CKD, the remaining working nephrons increase NH4 production and H+ secretion to counteract the failed nephrons, but overall production is decreased due to loss of kidney mass.
  2. Medullary interstitium has less NH3 because it has disrupted anatomy

These patients have a VERY acidic urine because of the lack of buffer

40
Q

What are the 3 major types of overdoses seen with acid gap metabolic acidosis?
Who do each typically affect?
What is a differentiating factor for each?

A
  1. Methanol intoxication- metabolized to formic acid that may cause visual impairments and hemodynamic instability. seen in alcoholics.
  2. Ethylene gycol (suicide or accident from drinking antifreeze)- metabolized to oxalate so a differentiating sign would be Caoxalate crystals in urine

(TREAT BOTH WITH ETHANOL/ DIALYSIS)

  1. Salicylates- aspirin OD with tinnitis and resp. alkalosis
41
Q

What is required for sustained metabolic alkalosis?

A
  1. Generation of the alkalosis - addition of non-volatile base or removal of non-volatile acid from the blood
  2. maintenance- the kidney needs to fail to correct the problem
42
Q

What are the 3 ways to generate a metabolic alkalosis?

A
  1. exogenous addition of base (baking soda or citrate ingestion, IV lactate, acetate, HCO3)
  2. GI acid loss (vomiting, NG suctioning)
  3. renal acid loss
43
Q

What are the 2 main situations when renal acid loss is the cause of the metabolic acidosis?

A
  1. Imbalance between distal Na delivery and mineralocorticoids (increased primary distal delivery via diuretics, osmotic diuretics, non-reaborbable anions)
  2. post hypercapneic alkalosis- in response to chronic respiratory acidosis, the kidney generates compensatory increase of HCO3. If CO2 corrects, there is metabolic alkalosis
44
Q

What are the 3 ways metabolic alkalosis is maintained by the kidneys?

A

The kidneys must either decrease the filtered load of HCO3, or increase the reasborption of HCO3 in the tubule.

  1. Volume depletion increases reabsorption AND decreases filtered load
  2. K deficiency- lowers GFR and increases proximal and distal H+ secretion
  3. increased aldo and distal delivery
45
Q

How can MOST metabolic alkalosis be treated?

What situations would not respond?

A

With saline to increase EABV thus not allowing the kidney to maintain the disturbance

primary Increased mineralocorticoids and hypokalemia would not respond to treating with volume

46
Q

When concerned that a patient may have metabolic alkalosis, what do you measure in the urine?

A

Cl <15mEq/L is suggestive of met alk. maintained by low EABV.

You measure Cl and not Na because a lot of ppl with metabolic alkalosis will have intermittent bicarbonaturia. This will give artifactually high Na

47
Q

You have a patient with low EABV and a Ucl of less than 15. What should their response to saline be?
What is maintaining the metabolic alkalosis?

A

The EABV is maintaining the alkalosis and they can be treated with saline.

48
Q

You have a patient with metabolic alkalosis. They have low EABV and a urine Cl greater than 15. What is this suggestive of?
Can you treat with saline?

A

This is suggestive of Low EABV + High distal delivery/mineralocorticoids.
They will be saline resistant

49
Q

You have a patient with metabolic alkalosis. They have a high EABV and a urine Cl> 15. What is the likely problem?
Can they be treated with saline?

A

They have high DDNA and high mineralocorticoids.

They will not correct with saline because the primary problem seems to be increased mineralocorticoids

50
Q

How does vomiting lead to metabolic alkalosis generation and maintenance?

A

Vomit decreases HCl which will increase bicarb, and decrease the volume.
There is so much bicarb generated, it causes bicarbonaturia which pulls out Na and K with it causing more volume depletion and hypokalemia.

Volume depletion –> aldosterone

The metabolic alkalosis is maintained by low K and low EABV.

51
Q

What is a situation where diarrhea could cause metabolic alkalosis instead of acidosis?

A

If the person has hereditary congenital chloridorrhea where the diarrhea has HCl in it

52
Q

How do diuretics cause metabolic alkalosis?

What happens when the patient is taken off diuretics but remains on a low salt diet?

A

High aldosterone due to decreased volume and high distal delivery lead to the metabolic alkalosis.
If the diuretics are stopped, but they remain on low salt diet, the alkalosis will be maintained because of continued volume contraction and K deficiency.

Saline infusion can correct this metabolic alkalosis.

53
Q

How does post hypercapneic alkalosis occur?

A

If the patient is maintaining CO2, the kidney will hold on the NaHCO3 as compensation. This leads to NaCl- diuresis and volume depletion.

When CO2 returns to normal, the low EABV will maintain the alkalosis

Renal (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions