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Nephrology > Acid-base disorders > Flashcards

Acid-base disorders Flashcards

1
Q

How does acid get excreted?

A 
- when combined with urinary buffers:
phosphate 
urate
creatinine
ammonia: major adaptive response is an increase in ammonim excretion in the urine
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2
Q

Buffers in our body?

A
  • respiratory
  • renal
  • carbonic acid bicarb buffer
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3
Q

How does resp buffer work?

A
  • pH will trigger an increase or decrease in rate and depth of ventilation until the approp amt of CO2 has been reestablished
  • compensation may occur within minutes
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4
Q

Respiratory compensation in metabolic acidosis and alkalosis?

A
  • metabolic acidosis: PCO2 will decrease by **1.3 mmHg every 1 mEq/L drop in serum HCO3 (better compensation in acidosis)
  • metabolic alkalosis: PCO2 will increase 0.7 mmHg for every 1 mEq/L increase in HCO3 (doesn’t increase that much b/c normal RR needs to be overriden to increase CO2)
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5
Q

Importance of bicarb?

A
  • base
  • buffer for H+ ions
  • renal system maintains balance of HCO3- and H+
  • there is small immediate change due to whole body buffering system
  • kidneys affect changes in pH which take 3-5 days (start chaging within 6-12 hrs with acute problem)
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6
Q

How much does bicarb buffer compensate in resp acidosis/alkalosis?

A
  • acute resp acidosis: HCO3 will increase 1 mEq/L per 10 mmHg increase in PCO2
  • chronic rep acidosis: HCO3 will increase 3.5 mEq/L per 10 mmHg increase in PCO2
  • acute resp alkalosis: HCO3 will decrease by 2 mEq/L per 10 mmHg decrease in PCO2
  • chronic resp alkalosis: HCO3 will decrease by 5 mEq/L per 10 mmHg decrease in PCO2
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7
Q

Main problem in respiratory acidosis?

A
  • too much CO2, resp drive? or CO2 exchange dysfxn
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8
Q

What are the causes of resp acidosis?

A
  • CNS depression: meds - (narcotics, sedatives, or anesthesia), or head injury
  • impaired resp muscle fxn: spinal cord injury, neuromuscular diseases, neuromuscular blocking drugs
  • pulm disorders: atelectasis, pneumonia, pneumothorax, pulmonary edema, bronchial obstruction, massive PE, respiratory failure
  • hypoventilation due to pain, chest wall injury/deformity, abdominal dissension, obesity trauma
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9
Q

Main problem in respiratory alkalosis?

A
  • hyperventilation

- tx by correcting underlying cause

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10
Q

Causes of resp alkalosis?

A
  • psych responses: anxiety or fear, pain
  • increased metabolic demands: fever, sepsis, pregnancy, or thyrotoxicosis
  • meds: resp stimulants
  • CNS lesions
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11
Q

What is the problem in metabolic acidosis?

A
  • not enough HCO3- to buffer acidic state of the body
  • HCO3- can be lsot: GI or renal losses
  • or too much acid can build up: excretion problem - renal failure, intake - overdose, metabolism issues: anaerobic, ketone bodies (DKA)
  • diarrhea, anaerobic metabolism: from tissue hypoxia
  • starvation
  • salicylate intoxication
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12
Q

What should you have at the top of your DDx when a pt has metabolic acidosis?

A
  • tissue hypoxia, look for hypoxic tissue
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13
Q

Anion gap calculation, normal range?

A
  • can be used to narrow down etiology of metabolic acidosis
  • AG = Na-(HCO3+Cl)
  • traditionally norm range 12+/- 4 mEq/L
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14
Q

What non acid-base disorders can cause errors in AG interp?

A
  • low albumin: for every 1 mEq/L decrease in serum albumin the AG will decrease by 2 mEq/L
  • hypernatremia
  • hyponatremia
  • certain abx
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15
Q

Why shoudl the AG always be calculated?

A
  • possible to have an abnormal AG even if Na+, Cl-, and HCO3- levels are normal
  • a large AG (greater than 20) suggests a primary metabolic acid-base disturbance regardless of pH or serum bicarb levels (not a resp problem)
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16
Q

What does a corrected HCO3 indicate?

A
  • in an increased AG acidosis there should be a mole for mole decrease in HCO3 as the AG increases
  • a corrected HCO3 higher or lower than normal (24) indicates the concomitant presence of metabolic alkalosis or normal AG gap metabolic alkalosis or normal AG gap metabolic acidosis
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17
Q

Causes of increased AG metabolic acidosis?

A 
MUDPILES:
M - methanol intoxication
U - uremia
D - diabetic or alcoholic ketoacdosis
P - paraldehyde
I - isoniazide or Fe overdose
L - lactic acid
E - ethylene glycol intoxication
S - salicylate overdose
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18
Q

causes of non-AG metabolic acidosis?

A

USED CAR:

U - ureteral sigmoid diversions: accum urine in intestine, reabsorb Cl-, H2O in intestine, secrete bicarb in intestine
S - small bowel fistula, saline admin
E - endocrinpathies: addison’s hyperparathyroidism
D - diarrhea
C - carbonic anhydrase inhibitors
A - (hyper) alimentation (TPA)
R - renal tubular acidosis

19
Q

What is the issue in metabolic alkalosis?

A
  • too much HCO3-: this can occur with excessive H+ loss, this can be GI or renal
  • or it can be from a gain in HCO3-
20
Q

Causes of metabolic alkalosis?

A
  • either an excess of base or loss of acid within the body
  • excess base occurs from ingestion of: antacids, excess use of bicarb, use of lactate in dialysis
  • loss of acids can occur secondary to:
    protracted vomiting, gastric suction, hypochloremia (bicarb isn’t getting exchanged with H+), excess admin of diuretics, high levels of aldosterone
21
Q

Sxs of alkalosis?

A
  • increased neuromusc irritability: paresthesias of fingers and toes, tetany, seizures
  • severe alkalosis: pt may become belligerent, CNS depression: confusion - lethargy, death at pH around 7.8
22
Q

How is H+ lost in metabolic alkalosis through vomiting? What happens normally?

A
  • each mEq of H+ lost generates 1 mEq of HCO3-
  • normally H+ is secreted into the stomach: when acidic chyme enters small intestine HCO3- is secreted into the lumen
  • person vomiting: H+ is being lost so HCO3- isn’t secreted
  • Cl- also secreted with H+ so lost with vomiting
  • so HCO3- doesn’t have H+ to bind to in the small intestine so it stays in the blood
23
Q

How is H+ lost with loop or thiazide diuretics with metabolic alkalosis?

A
  • increased flow to DCT and CT- increased reabsorption of Na+
  • as Na+ reabsorbed increased secretion H+ and increase HCO3- reabsorption
  • may also get volume contraction
24
Q

How does excess aldosterone cause increased H+ loss?

A
  • excess aldosterone is going to promote Na+ reabsorbtion and kick out H+ and increase HCO3- reabsorption
25
Q

What is contraction alkalosis? Causes?

A
  • loss of large volumes of fluid
  • contraction of extracellular vol around relatively quantity of bicarb
    causes: IV loop diuretics with rapid fluid removal,
    thiazides, vomiting (prolonged), sweat losses in pts with CF
26
Q

How can metabolic alkalosis be further characterized by urinary chloride?

A
  • can be diff in terms of response to tx with NaCl-

- by the level of urinary Cl as determined by ordering a spot or random UCI

27
Q

What does it mean if UCl is less than 10 mEq/L?

A
  • renal loss of chloride: diuretics, CF, posthypercapnia
  • GI loss of H+, Cl-:
    1. NG suctioning
    2. Vomiting
    3. chloride wasting diarrhea
    a. congenital in children
    b. villous adenoma
28
Q

What does it mean if UCl is greater than 10 mEq/L?

A
  • excess mineralocorticoid:
    1. adrenal: cushings, hyperaldosteronism (Conn’s syndrome)
    2. exogenous steroid admin
    3. bartter’s syndrome
29
Q

What is the initial problem in chloride sensitive metabolic alkalosis? What does this result in?

A
  • initial problem: sustained loss of chloride out of proportion to loss of Na (either by renal or GI)
  • this chloride depletion results in renal Na+ conservation leading to a corresponding reabsorption of HCO3- by the kidney
  • in this category of met. alkalosis: UCl - is less than 10 mEq/L
  • the disorders respond to tx with IV NaCl
30
Q

What is problem in chloride insensitive (resistant) metabolic alkalosis?

A
  • direct stim of kidneys to retain HCO3- irrespective of electrolyte intake and losses
  • UCl is greater than 10 mEq/L and these disorders don’t respond to NaCl admin
31
Q

What is the tx of metabolic alkalosis?

A
  • correct the underlying disorder
    1. chloride responsive:
    replace volume with NaCl if depleted
    correct hypokalemia if present
    admin of NH4Cl and HCl should be reserved for extreme cases
    2. chloride resistant: tx underlying problem, such as stopping exogenous glucocorticoids
32
Q

What can alklali admin cause?

A
  • milk-alkali syndrome
  • post correction metabolic alkalosis by admin of NaHCO3 to tx lactic acidosis or ketoacidosis
  • admin of large quantities of citrate (ex: with infusion of 8 or more units of blood or giving FFP in plasmapheresis)
    each mmol of citrate generates 3 mEq of bicarb (for a total of 23 meq of bicarb in each unit of blood)
  • metabolic alkalosis can occur if the renal ischemia or underlying renal disease prevents the excess bicarb from being excreted in the urine
33
Q

What does normal value of anion gap represent? range?

A
  • reflects concentration of nonbicarb buffers: albumin, phosphate, sulfate, organic acids
  • range 12+/- 4 but can be depending on the instrument used to measure serum electrolytes
34
Q

What is a high serum anion gap usually due to?

A
  • due to an increase in unmeasured anions and this is almost always caused by one of the organic metabolic acidoses (lactic acidosis, ketoacidosis, alcoholic acidosis)
35
Q

When should you use the delta gap equation?

A
  • only if anion gap is elevated for metabolic acidosis
  • it is the ratio of the increase in anion gap compared to the decrease in HCO3 concentration
  • AG measure - 12= delta AG
  • only will work with elevated AG
  • 24-measured HCO3= delta bicarb
36
Q

What does it mean if delta AG is greater than delta BC in metabolic acidosis?

A
  • metabolic alkalosis is present

- if equal (=/-2) then NO add disturbance)

37
Q

What does it mean if delta AG is less than delta BC?

A
  • then non-AG metabolic acidosis
    (for example: an add non-AG metabolic acidosis ( lactic acidosis superimposed on severe diarrhea)
  • if equal (=/-2) then no add disturbance
38
Q

How does normal rep compensation work in metabolic acidosis?

A
  • PCO2 should decrease by 1.3 mmHg for every 1 meq/L decrease in serum HCO3
  • PCO2 can only fall to 8-12 mmHg
39
Q

When do you use winter’s formula? Why is it used?

A
  • used in metabolic acidosis to predict the PaCO2 you should have if there is approp resp compensation for the metabolic acidosis
  • predicted PaCO2 =
    1.5x(HCO3-)+8(+/-2)
  • rough est is HCO3+15
    or PCO2 should be similar to decimal digits of pH (pH 7.25 the PCO2 should be about 25)
40
Q

What does a higher and lower than predicted winter’s formula mean?

A
  • higher than predicted: concomitant respiratory acidosis

- lower than predicted: concomitmant resp alkalosis

41
Q

How does norm. resp compensation work in metabolic alkalosis?

A
  • for every 1 meq/L elevation in HCO3 the PCO2 should increase by about 0.7 mmHg
  • upper limit for increasing the CO2 is about 55mmHg
42
Q

When is summer’s formula used? What do these values mean? Formula?

A
  • in metabolic alkalosis
  • it is used to calculate resp compensation (CO2) for metabolic alkalosis
  • if calculated CO2 is higher than actual= concomitant respiratory alkalosis
  • if calculated CO2 is lower than actual = concomitant respiratory acidosis
  • formula: PCO2 = 0.7(HCO3+21)+/-2
  • if normal than no resp compensation occurring
43
Q

When might it be helpful to measure a urine chloride?

A
  • metabolic alkalosis
44
Q

How long does it take for renal system to compensate by increasing the HCO3-?

A
  • 3-5 days, starts compensating in acute cases 6-12 hrs

Nephrology (15 decks)

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