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CPRII- Renal Exam > Acid-Base Disorders > Flashcards

Acid-Base Disorders Flashcards

1
Q

What are arterial and intracellular pH

A

Arterial: 7.35-7.45
Intracellular: 7.0-7.3

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2
Q

Most important extracellular buffering system

A

Bicarbonate buffer. HCO3- (basic, raises pH) and CO2 (acidic, lowers pH)

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3
Q

Where is carbonic anhydrase present?

A
  • Lung alveoli

- Renal tubular epithelial cells

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4
Q

What is the Henderson-Hasselbach equation?

A

pH=6.1 + log(HCO3/0.03xPCO2)

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5
Q

what organs alter the HH equation

A

Lungs
Kidneys

If one organ causes acidosis/alkalosis, the other organ will compensate

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6
Q

How do lungs regulate pH

A

Increase RR = blow off more CO2 = raise pH = alkalotic

Decrease RR = keep CO2 = lowers pH = acidodic

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7
Q

How do kidneys regulate pH

A

Excrete either an acidic or alkaline urine via either not reabsorbing HCO3 or secreting H+

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8
Q

What are the 4 kinds of acid-base disturbances?

A 
Metabolic Acidosis (low HCO3)
Metabolic Alkalosis (high HCO3)
Respiratory Acidosis (high PCO2)
Respiratory Alkalosis (low PCO2)
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9
Q

What are the 2 kinds of Met Ac

A

HAGMA

NAGMA (aka hyperchloremic)

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10
Q

What are the 2 kinds of Met Alk

A
  • Saline Responsive (hypovolemia; aka contraction alkalosis or chloride deficiency alkalosis)
  • Saline Non-Responsive (euvolemia or hypervolemia; rare)
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11
Q

How are acid-base disorders compensated?

A
  • Met Ac –> Resp Alk (lower PCO2; hyperventilate)
  • Met Alk –> Resp Ac (increase PCO2; hypoventilate)
  • Resp Ac –> Met Alk (increase HCO3)
  • Resp Ak –> Met Ac (decrease HCO3)
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12
Q

Normal ABG values?

A 
pH= 7.35-7.44
HCO3= 24 mEq/L
PCO2= 40 mmHg
Anion Gap= 12
Osmolality Gap= 10 mosm/kg
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13
Q

Acute and Chronic compensation for respiratory acidosis

A

Acute: HCO3 increases by 1 mEq/L for every 10 mmHg increase in PCO2 from normal (40)

Chronic: HCO3 increases by 3.5 mEq/L for every 10 mmHg increase in PCO2 from normal (40)

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14
Q

Acute and Chronic compensation for respiratory alkalosis

A

Acute: HCO3 decrease by 2 mEq/L for every 10 mmHg decrease in PCO2 from normal (40)

Chronic: HCO3 decrease by 5 mEq/L for every 10 mmHg decrease in PCO2 from normal (40)

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15
Q

How many AB disturbances can be present at once

A

3

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16
Q

Step-wise approach to acid-base problems

A
  1. Determine if acidosis or alkalosis is present
  2. Is it metabolic or respiratory? (metabolic=high or low HCO3, respiraotry= high or low PCO2)
  3. If metabolic acidosis, determine anion gap
  • Hypoalbunemia: calculate corrected anion gap
  • HAGMA: calculate osmolar gap, consider delta-delta gap
  1. Calculate compensation (red green schematic) for primary acid-base disorder. If adequate, it is simple acid base disorder. If not, mixed acid base disorder.
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17
Q

What does anion gap tell you?

A

“show whether your blood has an imbalance of electrolytes or too much or not enough acid. Too much acid in the blood is called acidosis. If your blood does not have enough acid, you may have a condition called alkalosis.”

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18
Q

What are the cations?

A 
Na+
K+
Ca+
Mg+
Protein + (not many)
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19
Q

What are the anions? What’s special about them?

A 
Cl-
HCO3-
Protein- (albumin!)
HPO4-
SO4 2-
Organic anions

They are buffered by H+ ions, which are buffered by HCO3-

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20
Q

How do you calculate anion gap and what’s the normal AG value?

A

AG= Na+ - (HCO3 + Cl)

Normal AG= 12+/- 2

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21
Q

How is AG used clinically i.e. what can it diagnose?

A
  • Differentiate between etiologies of metabolic acidosis (HAGMA or NAGMA)
  • Diagnose paraproteinemias (low AG)
  • Diagnose lithium, bromide, or iodide intoxication (low or negative AG)
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22
Q

If a pt has HAGMA, what could you next calculate?

A

Could calculate osmolar gap to screen for alcohol ingestion, ketoacidosis, lactic acisosis.

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23
Q

If AG>20, what should you be highly suspicious for?

A

Alcohol ingestion!!!

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24
Q

What is the equation for calculated serum osmolality?

A

2(Na) + (glucose/18) + (BUN/2.8)

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25
Q

What is the equation for osmolar gap?

A

Osmolar gap=measured serum osmolality-calculated serum osmolality

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26
Q

What is a normal and abnormal osmolar gap and what does it indicate?

A

Normal gap is < 10mosm/kg

If >10mosm/kg, suggests additional solutes in blood

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27
Q

When would you want to calculate a delta-delta gap?

A

To see if a pt w/ HAGMA has a coexistent NAGMA or metabolic alkalosis

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28
Q

How do you calculate delta gap?

A

Delta Gap = measured AG - normal AG

X - 12

29
Q

How do you calculate delta HCO3?

A

Delta HCO3 = normal HCO3 - delta gap

24 - delta gap

(remember that delta gap = measured AG - normal AG; X-12)

30
Q

For every increase in AG, there should be _____

A

an equal decrease in serum HCO3 due to HCO3 being buffered by H+

31
Q

What do the following values mean in regards to delta-delta gap?

  • HCO3 = 16
  • HCO3>16
  • HCO3<16
A
  • = 16: no additional disorder present; just HAGMA
  • > 16: HAGMA + metabolic alkalosis
  • <16: HAGMA + NAGMA
32
Q

HAGMA DDx (GOLDMARK)

A
  • Glycols (ethylene and propylene)
  • Oxoproline (pyroglutamic acid; acetaminophen toxicity)
  • L-lactic acidosis (normal isomer in anaerobic state)
  • D-lactic acidosis (malabsorption; short bowel)
  • Methanol
  • ASA
  • Renal Failure
  • Ketoacidosis (acloholic, DM, starvation)
33
Q

What is pryoglutamic (5-oxoproline) acidosis?

A

Seen in a malnourished or critically ill woman who takes a lot of Tylenol. Causes glutathione depletion leading to a shunting of glutamylcysteine to form pyroglutamic acidosis. We lose feedback inhibition.

34
Q

Dx and tx of pryoglutamic (5-oxoproline) acidosis?

A

Dx: urinary organic acid screen
Tx: Discontinue Tylenol, IVF, N-acetylcysteine

35
Q

NAGMA DDx (DURHAAM)

A
  • Diarrhea
  • Ureteral diversion (conduit) or fistula
  • Renal tubular acidosis (RTA)
  • Hyperalimentation (i.e. enteral feeding)
  • Acetazolamide (inhibits carbonic anhydrase)
  • Addisons Dz
  • Misc. (toluene toxicity from glue-sniffing)
36
Q

What does RTA mean? When can it NOT be dx?

A
  • Kidneys are having trouble excreting acid –> leads to NAGMA.
  • Could either be due to impaired H+ secretion or impaired HCO3 reabsorption
  • CANNOT dx in setting of AKI
37
Q

What are the RTA classifications?

A

RTA type 1 (distal)
RTA type 2 (proximal)
RTA type 4 (hyperkalemic; most common!)

38
Q

What results in RTA type 1 (distal)?

A

Decreased net H+ ion secretion in distal tubules and collecting duct

39
Q

What results in RTE type 2 (proximal)?

A

Decreased HCO3 reabsorption in proximal tubule

40
Q

What results in RTE type 4 (hyperkalemic)?

A

Decreased aldosterone secretion or aldosterone resistance leads to DECREASED net H+ and K+ secretion in collecting duct

41
Q

Which RTA’s have an abnormal UAG (i.e. a positive value)?

A

RTA 1

RTA 4

42
Q

What is UAG (urine anion gap) used for?

A

To differentiate between renal (RTA) and non-renal causes of NAGMA

43
Q

What is UAG a marker of?

A

Marker of NH4Cl excretion which indicates appropriate urinary acidification. In setting of met ac., urinary NH4Cl excretion should increase to get rid of extra acid. But if something is wrong w/ the kidneys, won’t be getting rid of extra acid.

44
Q

How is UAG calculated?

A

UAG = (Urina Na + Urine K) - Urine Cl

45
Q

What do negative and positive UAG values mean?

A
  • Negative: appropriate distal nephron urinary acidification (RTA 2 proximal)
  • Positive: inappropriate distal nephron urinary acidification (RTA 1 distal and 4 hyperkalemic)
46
Q

Dx:

Suspected RTA
Hypokalemia
Has proximal tubular dysfx (aminoaciduria, phosphaturia, glucosuria, bicarbonaturia i.e. fanconi, tubular proteinuria, uricosuria)

A 
RTA 2 (proximal)
UAG will be negative (normal) but it CAN be positive (abnormal)
47
Q

Dx:

Suspected RTA
Hypokalemia
No proximal tubular dysfx

What is impaired in this RTA?

A 
RTA 1 (distal; impaired H+ secretion)
UAG is positive (abnormal)
48
Q

Dx:

Suspected RTA
Hyperkalemia

when is this most often seen?

A 
RTA 4 (hyperkalemic)
UAG is positive (abnormal)

seen in DM2 or CKD

49
Q

What are signs of proximal tubular dysfx i.e. Fanconi syndrome? GAP BUT

A
  • Glucosuria
  • Aminoaciduria
  • Phosphaturia
  • Bicarbonaturia (proximal RTA 2)
  • Uricosuria
  • Tubular proteinuria
50
Q

Increased osmolar gap DDx? (remember: you measure this if a pt has HAGMA to r/o alcohol ingestion)

MEDIE

A
  • Methanol
  • Ethanol
  • Diethylene glycol ( diuretic mannitol)
  • Isopropyl alcohol (rubbing alcohol; pt will have increased AG but no metabolic acidosis!!!)
  • Ethylene glycol (antifreeze)

-also propylene glycol and ketoacidosis and lactic acidosis

51
Q

What can methanol (aka moonshine) ingestion lead to?

A

Leads to metabolism of formaldehyde to formate which can cause blindness

52
Q

What can ethylene glycol ingestion lead to?

A

Leads to production of glycoxylic acid –> oxalic acid (can cause renal failure)

53
Q

In what pt should you monitor for HAGMA associated w/ increased osmolar gap?

A

A pt who is on a benzo drip b/c propylene glycol is the solvent used to deliver lorazepam and diazepam

54
Q

Acidosis is associated w/ K+ level?

A

HYPERKALEMIA!

55
Q

What ions enter/leave the cell in acidosis associated w/ hyperkalemia?

A
  • Acidosis: H+ enters, K+ exits
  • Hyperkalemia: K+ enters, H+ leaves

These both happen in order to maintain neutrality!

56
Q

Alkalosis is associated w/ what K+ level?

A

HYPOKALEMIA!

57
Q

What ions enter/leave the cell in acidosis associated w/ hypOkalemia?

A
  • Alkalosis: H+ exit, K+ enters

- Hypokalemia: K+ exit, H+ enters

58
Q

What can lead to a metabolic alkalosis, in general?

A

Anything that increases Na+ reabsorption will secondarily increase H+ secretion (b/c need to keep neutrality), causing HCO3- reabsorption potentially leading to a metabolic alkalosis

59
Q

Metabolic Alkalosis DDx

A
  • Hypokalemia
  • Vomiting or NG tube suctioning
  • Loop and thiazide diuretics
  • Volume depletion (contraction alkalosis leads to RAAS activation and aldosterone secretion which worsens alkalosis)
  • Mineralocorticoid excess
60
Q

Resp. Alkalosis DDx

A

Anything that increases RR or tidal volume!

  • PNA
  • PE
  • Pulmonary edema
  • PTX
  • Sepsis
  • CHF
  • Anxiety, pain, fever
  • Salicylates
  • Exercise
  • Trauma
61
Q

Resp. Acidosis DDx

A

Anything that lowers RR, tidal volume, increases dead space, or worsens airway obstruction. Inadequate vent settings. Increases in CO2 production (high carb diet, hyperthermia, seizures)

  • Diaphragmatic weakness due to hypo/hyperkalemia
  • ARDS
  • PNA
  • PE
  • ILD
  • Fx ribs
  • COPD or asthma
  • Benzos, opiates
  • Central brainstem lesion
62
Q

___ secretion leads ____ reabsorption

A

H+ secretion leads HCO3- reabsorption

63
Q

Etiology, clinical sx, and dx of RTA 2 proximal?

A

Etiology:

  • MC in children w/ cystinosis
  • Most adults w/ Fanconi syndrome have MM

Sx:
-Mild hypokalemia compared to RTA 1 distal

Dx:

  • Urine pH can be high or low depending on sHCO3 level; can be <5.5 when in new steady state
  • UAG is negative: normal
64
Q

What causes the decreased H+ secretion in RTA 1 distal?

A
  • SOmething wrong w/ H/K ATPase or H/ATPase effect
  • Gradient effect: abnormally permeable distal tubule and collecting duct allows secreted H+ ions to flow back into tubular cell; due to amphotericin for fungal infxn
65
Q

Etiology, clinical sx, and dx of RTA 1 distal?

A

Etiology:

  • Sjogrens
  • GLue sniffing

Sx:
-Nephrolithiasis or nephrocalcinosis

Dx:

  • NAGMA
  • Unable to acidify urine <5.5
  • Severe hypokalemia
  • UAG positive: abnormal
66
Q

RTA 4: what can cause deficiency of aldosterone?

A 
DM
Drugs (NSAIDs, beta blockers, ACEiARB, high dose heparin)
67
Q

RTA 4: what can cause aldosterone resistance?

A
  • Interstitial renal dz

- Drugs (amiloride, triamterene, sprinolocatone, trimethoprim)

68
Q

Clinical sx and dx of RTA 4 hyperkalemia

A

Sx:

  • Usually asx
  • Hyperkalemia
  • Oler pt’s w/ DM or CKD

Dx:

  • Urine pH usually >5.5
  • Positive UAG: abnormal

CPRII- Renal Exam (6 decks)

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