Renal: Acid-Base

Front 1

Volatile acid:
1) what is it?
2) why is it called volatile?
3) how much is made per day?

Back 1

1) H2CO3
2) CO2 excreted by lungs
3) 15,000 mmol = 15 moles

Front 2

Non-Voatile acids:
1) what are they (2)?
2) how are each of these produced
3) How much is made per day

Back 2

1) H2SO4 and H3PO$
2) H2SO4 is made from AA metabolism (esp. methionine)
H3PO4 is made from phospholipid oxidation
3) 1 meq/kg/day = 50-100 meq/day

Front 3

Organic acids:
1) what are they (2)?
2) how are each of these produced

Back 3

1-2) Lactic acid- made from anaerobic glycolysis
Beta-hydroxybutyric acid- made from anaerobic oxidation of Fatty acids

Front 4

After CO2 is produced from metabolism, it combines with__1__ to form ___2__ which then dissociates to __3__ and __4__. __4___ then is buffered by __5__ which has pKa of __6___.

Back 4

1) water
2) H2CO3
3) HCo3-
4) H+
5) Hemogobin
6) 7.4

Front 5

pKa of Hemoglobin?

Back 5

7.4

Front 6

Three meothods of compensation for acidosis

Back 6

respiratory- tachypnea
renal- reclaim bicarb
Bone buffering- liberate H2PO4 from hydroxyapatite

Front 7

Three changes made by kidneys in response to acid load and how these changes are accomplished.

Back 7

1) reclamation of filtered HCO3- in the PCT
2) ammoniagenesis enzymes upregulated to titrate acid in urine
3) de-novo generation of HCO3 in alpha- intercalated cells in the CD by upregulating HCO3-/Cl- exchangers and apical H+ exporters to traffic the products of carbonic acid dissociation

Front 8

1) which type of cells in the CD are responsible for de-novo bicarb generation
2) what channels do they have critical for this process?

Back 8

1) alpha- intercalated cell
2) Basal bicarb/Cl- exchanger (pumps bicarb into blood)
3) apical H+ exporters

Front 9

How does bone buffering work?

Back 9

H+ stimulated release of H+ by osteoclasts onto bone matrix

Front 10

define:
1) acidemia
2) alkalemia
3) acidosis
4) alkalois

Back 10

1)pH <7.36
2)metabolic or respiratory process that tends to move pH down from 7.4
3)pH>7.44
4) metabolic or respiratory process that tends to move pH up from 7.4

Front 11

complete acid/base compensation suggests?

Back 11

second primary acid/base disorder

Front 12

define formula for anion gap

Back 12

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

Front 13

Components which make up the normal anion gap

Back 13

Anions of mineral acids
pyruvate, lactate, Beta-hydroxbutyrate, oxlalte, formalate
albumin (75%)

Front 14

3 Causes of an elevated anion gap:
general

Back 14

1) retention of mineral acids during severe renal failure
2) generation of lactate and Beta-hydroxybutyrate during metabolic stress or ingestion of a toxic acid precursor
3) inclusion of lactate or sodium citrate in IV therapy

Front 15

3 causes of a decreased anion gap:
general

Back 15

1)decreased serum albumin
2)serum dilution
3)increased + charged protein as in multiple myeloma

Front 16

serum osmolal gap
1) definition (non math)
2) use
3) common causes of elevation

Back 16

1) difference between calculated and measured serum osmolaity
2) suggests amount of non-electrolyte solute, especially those likely to be metabolized to organic acids
3)EtOH, IprOH, Ethylene Glycol, Methanol, Mannitol

Front 17

Main criteria that we use to sub-divide metabolic acidosis

Back 17

Elevated anion gap or not

Front 18

Causes of anion gap metabolic acidosis

Back 18

any acid generated that titrates HCO3- leaving a replacement anion that is not measured--
organic or mineral acids

Front 19

Causes of non-anion gap metabolis acidosis

Back 19

Any acid generated which titrates HCO3 leaving a measured anion in its place eg. HCl ingestion
OR
reabsorbtion of Cl- inctead of HCo3 in the kidney (Renal tubular acidosis)
OR
GI secretory disorder wherein abnormal amounts of HCO3- are secrete, and in its place Cl- is absorbed accompanied by H+

Front 20

1) define renal tubular acidosis
2) does it cause an anion gap?

Back 20

1) kidney reabsorbs Cl- instead of HCO3-

2) No-- Cl- is a measured anion

Front 21

4 common ingestions which an cause metabolic acidosis and the acids that they lead to.

Which One causes an elevated Anion Gap?

Back 21

aspirin--> salicylate, lactate
Ethylne glycol--> glycolate, oxalate
MeOH--> formate
Acetaminophen--> lactate due to liver injury (Anion Gap)

Front 22

Two main cases of non-ingestion anion-gap acidosis due to acid production

Back 22

lactic acidosis
ketoacidosis

Front 23

This acid/base status suggests Renal tubular acidosis or a GI secretory disorder

Back 23

non-anion gap metabolic acidosis

Front 24

Renal failure causes a metabolic Acidosis:
1) How?
2) AG?

Back 24

1) mineral acid retention
2) Yes- anion gap

Front 25

How can these things cause Lactic Acidosis?
1)Cardiogenic shock
2) Liver Failure
3) Sepsis and Shock

Back 25

1) ischemia causes anaerobic glycolysis and hypoperfusion of liver disallows detoxification of Lactate
2)Blood flow shunted away from liver decreases its ability to detoxify lactate. This is combines with insufficient Hepatic glycogen which results in hypoglycemia and further lactic acidosis.
3) E.Coli and other bacteria can directly produce lactate. Also, shock causes hypoperfusion and thus encourages anaerobic metabolism.

Front 26

Three causes of ketoacidosis.

Back 26

Diabetic Ketoacidosis
Starvation Ketoacidosis
Alchoholic Ketoacidosis

Front 27

Describe the mechanism by which ketoacidosis evolves.

Back 27

low insulin allows adipocyte production of FFAs. These are metabolized in the liver (due to high glucagon and low insulin) to ketone bodies.

Front 28

How does salicylism cause Lactic acidosis?

Back 28

uncouples H+ ATPase and dissipates. proton gradient. With the resultant ATP shortage, the body must rely on anaerobic glycolysis.

Front 29

Salicylism:
Symptoms

Back 29

Lactic acidosis
Increased Respiratory Drive
Neuro Symptoms- vertigo, nausea, seizures
Also causes release of cytotoxic glutamate

Front 30

Aside from metabolic acidosis, what other symptom does Ethylen glycol toxicity produce?

Back 30

Renal failure and CNS toxicity due to Calcium oxalate stone formation

Front 31

When biarbonate become scarce due to leakage from the GI tract, how does the body compensate and why?

Back 31

Reabsorbs Cl- to maintain electroneutrality.

This causes Non-anion gap acidosis

Front 32

Deep respirations occuring during compensation for metabolic acidosis are called

Back 32

Kussmaul's respiration

Front 33

During compensation for metabolic acidosis, we can predict the respiratory compensation numerically. How?

Back 33

PCO2= 1.5 x [HCO2] + 8 +/-2

Front 34

Renal response to a metabolic acidosis is quantitatively dominated by what process?

Back 34

ammoniagenesis

Front 35

Metabolic alkalosis can be initiated by three things

Back 35

1) increased reclamation
2) increased renal production (beta-intercalated cell)
3) increased gastric production
(parietal cell)

Front 36

Regardless of initiating event, metabolic alkalosis requires what change in the kidney to be maintained?

Back 36

Raising tubular maximum for Bicarb reabsorption or it would all be spilled out quickly.

Front 37

Two categories of metabolic alkalosis

Back 37

saline responsive (contration) alkalosis and saline unresponsive alkalosis

Front 38

What causes saline responsive (contraction alkalosis)

Back 38

Loss of H+ or K+ rich fluid

Front 39

1) how does loss of K+ cause a saline responsive metabolic alkalosis?
2) Does urinary chloride go up or down in saline responsive metabolic alkalosis? why?
3) treatment?

Back 39

1) Depletion of cellular K+ triggers the H+/K+ exchanger. This causes acid loss in order to retain K+. Also in order to reclaim K+, massive ammoniagenesis is initiated, which causes acid titration in urine.

2) down-- body is trying to retain all ions possible
3) K+ and volume repletion

Front 40

1) What causes saline unresponsive metabolic alkalosis?
2) Mechanism?
3) Does urinary chloride go up or down in saline unresponsive metabolic alkalosis? why?
4) treatment?

Back 40

1) Primary increase in mineralocorticoids.
2) Na+ reclamation causes hypokalemia. Depletion of cellular K+ triggers the H+/K+ exchanger. In order to reclaim K+, massive ammoniagenesis is initated, which causes acid titration in urine.
3) Up to remain in salt balance
4) K+ and mineraocorticoid receptor antagonist

Front 41

initiators of metabolic acidosis

Back 41

loss of gastic acid through vomiting or NG tube
Massive antacid ingestion
IV bicarb during cardiac resuscitation
Loop diuretics
Post hypercapnic state
Mineralocorticoid excess

Front 42

Maintainers of Metabolic acidosis

Back 42

Volume depletion (vomiting, diuretics)
Renal insufficiency (cant remove addec bicarb)
Mineralocorticoid excess

Front 43

Causes of respiratory acidosis: Give examples
1) inhibition of brainstem resp. drive
2) disorders of respiratory muscles or chest wall function
3)upper airway obstruciton
4) Depressed alveolar gas exchange

Back 43

1) CNS depressants, post Cardiac arrest, sedatives, benzodiazepines, opiates
2)neuropathy, Myasthenia gravis, obesity, chest wall deformation
3) forgein body, laryngospasm, OSA, asthma
4) COPD, pulmonary edema

Front 44

Causes in respiratory alkalosis

Back 44

Sensations of SOB, hypoxia, anxiety, severe pain, severe liver disease with hepatic encephalopathy, salicylate toxicity

Front 45

How does one get a combined metabolic and respiratory acidosis?

Back 45

Severe, prolonges sepsis, or CHF
Sepsis- E. coli produce lactate and shock cause shunting from kidney and liver. Also, causes respiratory failure.

CHF- poor perfusion causes lactate buildup. Pulmonary edema causes CO2 retention.

Front 46

How does one get a respiratory acidosis combined with a metabolic alkalosis?

Back 46

patient with COPD who chronically retains CO2 (respiratory acidosis) is treated with EITHER a glucocorticoid (which has crossover mineralcorticoid activity) or a diuretic. These drugs cause K+ loss which results in attempted K+ retention leading to H+ secretion (metabolic acidiosis). This low K+ state contributes to dysfunction of the bellows muscles, worsening respiratory alkalosis.

Front 47

How does one get a respiratory alkalosis combined with a metabolic acidosis?
1) salicylism
2) liver failure
3) how is #2 complicate to cause the "triple threat" acid/base picture

Back 47

Salicylism causes a lactic acidosis (anion gap). Mitochondiral uncoupling is interpreted by the central chemoreceptors as tissue hypoxia, driving tachypnea leading to a respiratory alkalosis.

OR

2)Liver failure causes uremic or lactic metabolic acidosis to develop acutely. Concurrent inability to convert NH3 to urea results in CNS intoxication and increases ventilatory drive to improve NH3 volatilization.
(respiratory alkalosis)

3) In sever liver failure, the above picture (R-alk, M-acid) an be complicated by vomiting which causes a Metabolic alkalosis.

Front 48

Predicted compensations for:
Metabolic Acidosis

Back 48

1.2mmHg decrease in PCO2 per 1mEq decrease in [HCO3]

Front 49

Predicted compensations for:
Respiratory alkalosis

Back 49

5meq/L decrease in [HCO3] for

Front 50

Predicted compensations for:
Metabolic Alkalosis

Back 50

0.7 mmHg increase in PCO2 for every 1mmHg increase in [HCO3]

Front 51

Predicted compensations for: Respiratory Acidosis

Back 51

3.5 meq/L increase in [HCO3] per 10 mmHg increase in PCO2

Front 52

1)how do we treat a severe acute metabolic acidosis?
2) how do we treat a mild CHRONIC metabolic acidosis.
3) how do we treat a mild acute Lactic metabolic acidosis? Why?

Back 52

1) IV Bicarbto raise pH to 7.2
2) Oral bicarb to raise [HCO3] to 21-22
3) We dont give bicarb. We work to correct the underlying cause of the acidosis. This is because once we do, the lactate will be metabolized to Bicarbonate, which will self-titrate the extra acid. Exogenous bicarb would cause overshoot which can give a quick rise in pH, shifting the oxyhemoglobin curve to the left. depriving already stunned tissues of oxygen.