Brainscape's Knowledge GenomeTM

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


See full index

MS2 Renal > 9/8- Intro to Acid Base Disturbances > Flashcards

9/8- Intro to Acid Base Disturbances Flashcards

1
Q

Normal values for arterial blood:

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

Normal values for venous blood:

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

What are the main sources for acid in the body?

A
  • Diet (20 mmol H/day)
  • Metabolism (H as nonvolatile acids 40 mmol/day)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How much acid is excreted per day?

A

About 70 mmol H+ is excreted in the urine/day

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

How is pH regulated (constantly)?

A

Buffers

  • Absorb hydrogen ions when in excess and can release if depleted
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the largest buffering system? Others?

A

Largest = bicarbonate

  • Bicarbonate content can be regulated by the kidney and respiratory drive

Others: phosphates, proteins, hemoglobin…

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

Bicarbonate buffer system equation

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

Addition of acid leads to low levels of what?

A

Bicarbonate

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

What is the Henderson Hasselbach equation for bicarbonate buffer system?

A
  • Typically pH and pCO2 are measured from arterial stick and then HCO3- is calculated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the cardinal acid base disorders and what can cause them?

A
  • Metabolic acidosis (addition of acid, loss of bicarbonate)
  • Metabolic alkalosis (addition of alkali, loss of acid)
  • Respiratory acidosis (retention of CO2/ventilatory failure)
  • Respiratory alkalosis (loss of CO2/hyperventilation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Note: PCO2 levels from ventilation/respiratory compensation is always in the same direction as HCO3 (high acid accumulation with low HCO3 levels means PCO2 must be lowered as well, with hyperventilation.. and vice versa)

A

(:

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

How does the kidney compensate for accumulated PCO2?

A

Increased bicarbonate (HCO3) retention

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

What is the diagnosis (metabolic/respiratory acidosis/alkalosis) for:

  • Arterial pH = 7.20
  • HCO3- = 14 meq/L
  • pCO2 = 30 mmHg
A

Metabolic acidosis (plug into H-H)

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

What is the diagnosis for:

  • Arterial pH = 7.42
  • HCO3- = 35 meq/L
  • pCO2 = 60 mmHg

A. Metabolic acidosis

B. No disturbance

C. Metabolic acidosis and respiratory acidosis

D. Metabolic alkalosis and respiratory acidosis

A

Have normal pH but abnormal values (think mixed disorders)

  • Always start with pCO2; it is high, so respiratory acidosis

D. Metabolic alkalosis and respiratory acidosis

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

How does the kidney handle H and HCO3?

  • Proximal acidification
  • Titrable acids and ammonia
  • Distal acidification
A

Proximal acidification:

  • Bicarbonate reabsorption
  • No acid excretion

Titrable acids and ammonia:

  • Acid excreted

Distal acidification:

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

What defects may lead to proximal renal tubular acidosis?

A
  • Defect in Na-H exchange (NHE)
  • Defect in carbonic anhydrase enzyme

Threshold of bicarbonate reabsorption reduced

  • Extremely difficult to “normalize” serum bicarbonate level with supplements
17
Q

What is the main goal of the proximal tubule in terms of acid-base equilibrium?

A

Bicarbonate reabsorption

  • No acid excretion in this process
18
Q

Proximal tubular damage leads to what?

A
  • Bicarbonaturia
  • Glycosuria
  • Aminoaciduria
  • Phosphaturia (Fanconi’s)
19
Q

What are some causes of proximal RTA?

A
20
Q

What is fractional excretion (FE)?

A

Amt excreted / amt filtered

21
Q

Where does ammoniagenesis happen?

A

Mostly in proximal tubule, but other places as well

22
Q

What is the main titratable acid?

A

HPO4- (can accept hydrogen and be excreted as H2PO4)

23
Q

How does the kidney account for acid overload?

A
  • Titrable acid excretion
  • Ammoniagenesis
24
Q

Action of the distal nephron with classic or Type I RTA?

A
  • Defective intercalated cell: protons not pumped or they back-leak into blood Effect of Distal RTA:

—Tubule lumen more negative

—Potassium excretion enhanced

—Urine not acid

  • Acid accumulates over time, and very low HCO3 levels can occur
  • Bone buffers acid, causing osteoporosis, hypercalciuria, and kidney stones
  • Very low serum potassium levels
25
Q

Distal RTA and stones

A
  • Acidemia leads to release of calcium phosphate from bone (buffer)
  • Acidosis leads to retention of citrate in proximal tubule – ↓ citrate in urine
  • High urine pH: precipitation of calcium phosphate stone
26
Q

____ is a natural inhibitor of stone formation

A

Citrate is a natural inhibitor of stone formation

27
Q

Causes of distal RTA

A

Idiopathic Familial

  • Autosomal dominant and recessive

Secondary

  • Rheumatologic (RA, Sjogren’s, SLE)
  • Drugs (Amphotericin B, Ifosfamide, Lithium)
  • Renal transplantation
  • Others: cirrhosis, sickle cell anemia etc
28
Q

What can cause Hypo-renin hypo-aldosteroneism (Type 4) RTA?

A
  • Originally described in diabetics

Other causes:

  • Urinary obstruction
  • Medications (Bactrim, K-sparing diuretics)
  • Renal interstitial inflammation

—-Allergic interstitial nephritis

—-Systemic lupus erythematosus

Originally though to be due to low aldosterone state

29
Q

What is seen in Hypo-renin hypo-aldosteroneism (Type 4) RTA?

A

Principal cell sodium channel defect:

  • Tubule lumen not negative
  • Hyperkalemia ensues

Hyperkalemia inhibits proximal NH4+ production and bicarbonate generation falls

Thus patients appear to have hypoaldosteronism (one of many etiologies Type IV RTA)

30
Q

Summary slide

A
31
Q

What is the urine “anion gap”? What causes a negative or positive gap?

A

Urinary (Na + K) should = urinary Cl

  • Urine NH4 is not directly measured

“Negative urine gap”: Cl > (Na + K)

  • NH4 production increased in response to acidosis (e.g. diarrhea)

“Positive” gap:

  • NH4 absent (e.g. failure of kidney to make ammonium); RTA
32
Q

Case)

  • 60 yo male present with new onset of glucose in the urine
  • Tired and his bones “hurt”

Labs:

  • Arterial pH = 7.29
  • HCO3- = 16 meq/L
  • Anion gap = 10 (normal 10-12)
  • Urinalysis = 3+ glucose

What is his diagnosis?

A. Distal RTA (type I)

B. Proximal RTA (type 2)

C. Hyperkalemic RTA (type 4)

A

A. Distal RTA (type I)

B. Proximal RTA (type 2)

C. Hyperkalemic RTA (type 4)

  • Acidemia
  • Low HCO3, so possibly metabolic acidosis
  • Proximal RTA affected (glucose in urine)
  • Giving this pts bicarbonate will not increase levels significantly
33
Q

Case)

  • 24 yo female
  • Referred for abnormal lab values
  • She also has a rheumatologic disease

Labs:

  • Urine pH = 6.5
  • HCO3- = 8 meq/L
  • Anion gap = 10 (normal)
  • Potassium (2.9 meq/L)

What is her diagnosis?

A. Distal RTA (type 1)

B. Proximal RTA (type 2)

C. Hyperkalemic RTA (type 4)

A

A. Distal RTA (type 1)

B. Proximal RTA (type 2)

C. Hyperkalemic RTA (type 4)

  • Urine pH can vary from 4.5 - 7 based on diet
  • Serum bicarb is VERY low… so urine pH should be very low (instead it is high)
  • Inability to acidify the urine

MS2 Renal (25 decks)

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