Metabolic Acidosis and Alkalosis Flashcards
1
Q
what are the two main mechanisms for developing a metabolic acidosis?
A
- extrarenal processes
- increased acid production
- accelerated extrarenal loss of HCO3
- primary defect in renal acidification. this is a defect within the tubules of the kidney itself, which are either:
- having _trouble regeneratio_n enough HCO3 to replace that being lost in buffering acid
- seen in distal RTA
-
losing filtered HCO3 in the proximal tubule
- see in proximal RTA
- reabsorbing too much H+ alongside increased Cl- reabsorption
- __this can be seen when patients are administered saline. normal saline has a much higher [Cl-] than plasma, and will induce concomitant Cl-/H+ reabsorption, causeing a Hyperchloremic Metabolic Acidosis
- having _trouble regeneratio_n enough HCO3 to replace that being lost in buffering acid
RTA = Renal Tubular Acidosis
2
Q
what pH is considered metabolic acidosis?
what will a metabolic panel & ABG (arterial blood gas) of metabolic acidosis show?
A
- ph < 7.36
- metabolic profile: shows reduced [HCO3-]
- ABG: usually shows a pCO2 < 40 mmHg (due to respiratory compensation)
3
Q
- what is an anion gap and how does it characterize different types of metabolic acidosis?
A
- the degrees of anion gap in metabolic acidosis are dictated by whether or not the accumulating acid contains Cl- (i.e., whether or not the accumulating acid is HCl)
- accumulating acid is HCl: causes
-
normal anion gap acidosis
- hyperchloremic metabolic acidosis
-
normal anion gap acidosis
- accumulating acid contains an anion other than Cl-: causes
- high anion gap acidosis
- accumulating acid is HCl: causes
4
Q
- how to calculate anion gap?
- what is a normal anion gap?
- why is this the case?
A
- anion gap is calculated from electrolytes measured in the lab
- Na+, Cl-, HCO3
- put into the equation:
- Na+ - [Cl- + HCO3-]
- normal anion gap: 12
- this gap represents the number of unmeasured anions in circulation, which exceeds that of unmeasured cations
5
Q
- which unmeasured anion is the largest contributer to the anion gap?
- what does this mean clinically?
A
- albumin
- normal albumin level is 4.
- someone’s anion gap is roughly 3x their albumin level - hence, a normal anion gap is 12
- however, in the setting of hypoalbuminema (perhaps due to cirrhosis, glomerulonephritis, protein wasting enteropathy), the lower albumin level will result in a lower anion gap, resetting the normal anion gap to something below 12
6
Q
- what are unmeasured anions that would cause a high anion gap metabolic acidosis?
- what is the status of calcium in this setting?
A
i.e., an anion gap > 12. [Cl-] in case is normal. other anions are causing the gap:
- M - methanol
- U - uremia
- L - lactic acidosis (Type A = L-Lactic Acidosis, Type B= D-Lactic acidosis)
- E - ethylene glycol
- P - paraldehyde
- A - alcoholics
- K - ketones (see in DKA & starvation)
- S - salicylates
7
Q
physiological states that create high anion gap
A
- Metabolic acidosis, metabolic alkalosis, respiratory alkalosis
- Lab Error- if you cannot determine a cause within MULEPAK, might be an error
- Severe volume depletion: hyper- albuminemia can occur as body’s attempt to conservate water, and since anion gap is 3x albumin, this will increase anion gap.
- severe hyperphosphatemia - addition of an unmeasured anion that usually isn’t present in high amounts
- I_ncreased anionic paraproteins_ (IgA Myeloma)
8
Q
assessment of HCO3. it pt definitively has a low serum [HCO3-], what steps do we take to narrow down their diagnosis?
A
- 1st: make sure the reason for the low HCO3- is metabolic acidosis instead compensated respiratory alkalosis (i.e. chronic resp. alkalosis)
- do this by checking ABG.
- 2nd: calculate anion gap (Na - Cl - HCO3)
-
if anion gap is normal:
- check urine anion gap:
-
+ urine anion gap: suggests renal origin
- RTA (Type I, Type II, Type IV)
-
- urine anion gap: suggests GI loss
- diarrhea
- pancreatic losses
- biliary secretions
-
+ urine anion gap: suggests renal origin
- check urine anion gap:
-
if anion gap is high:
- MULEPAK
-
if anion gap is normal:
9
Q
- walk through how to classify various types of acidosis based on anion gap, and renal vs suprarenal origin.
A
- this is same process assess
10
Q
lactic acidosis
- causes what kind of metabolic acidosis?
- what are the variations of lactic acidosis & what causes them?
A
- lactic acidosis causes a high anion gap metabolic acidosis
- Type A (L- Lactic acidosis_
-
due to hypoxia, often because of
- hypoperfusion (from cardiac failure)
- anemia
- carbonx monoxide posoining
- COPD
-
due to hypoxia, often because of
- Type B (D-Lactic Acidosis)
-
due to cell injury
- liver failure/renal failure
- exercise trauma that injures cells
- seizure
- thiamine deficiency
- metformin (common cause**)
- alcohol in malnourished
- cancer
-
due to cell injury
- Type A (L- Lactic acidosis_
11
Q
what are the causes of a low/negative anion gap?
A
a low/negative anion gap is extremely rare.
- causes
- lab error (most common)
-
hypoalbuminema (second most common)
- in this case, the person’s low anion gap is considered to be their respective “normal”
-
cation imbalances (third most common)
-
an increase in unmeasured cations
- __monoclonal/polyclonal gammopathy
- i.e. IgG myleoma (IgG is a cation)
- bromide (Br+), lithium (Li) , Ioidide (I) toxicity
- severe hypercalcemia
- severe nypermagnesemia
- __monoclonal/polyclonal gammopathy
-
Low Na+ with SIADH
- __b/c Na is a measured cation & plugging this into teh equation lowers the gap
-
an increase in unmeasured cations
12
Q
major causes of a normal anion gap (non-gapped) metabolic acidosis
A
aka, hyperchloremic acidosis
- extrarenal losses:
-
often GI losses:
- diarrhea
- pancreatic/billary losses
- surgeries - uterosigmoiostomy/jejunal loop
-
drugs:
- that contain high amounts of HCl/NH4Cl
- CaCl
- fluids - example, saline (has high HCl)
- that induce diarrhea & thus cause base loss:
- MgSO2 (osmotic agent)
- cholestyramine (bile acid sequestrant)
- that contain high amounts of HCl/NH4Cl
-
often GI losses:
- renal losses (renal tubular acidification defects)
-
Hypokalemic defects:
- Type I RTA (proximal RTA) - decreased HCO3 reabsorbed in PT
- Type II RTA (distal RTA) - impaired H+ secretion in DT
-
Hyperkalemic defects: associated w/ decreased secretion of aldosterone (or mineralcorticoids - have same effect as aldosterone)
- type IV RTA - associated with aldosterone deficiency: stimultaneous retention of H+/K+
- mineralcorticoid deficiency - presents w/ HTN
- mineralcoriticoid resistance - presents w/ HTN
- decreased tubular Na+ delivery to distal nephron - aldosterone not activated, K+ retention
-
Hypokalemic defects:
13
Q
try to fill this out. i have explanations for some things on the back of the card but don’t get your hopes up.
A
- by definition, “hyperchloremic acidosis” = normal anion gap acidosis. all these will have a normal anion gap.
- remember that all renal losses (the RTAs) result in a low (-) urine anion gap, which is why you can tell them apart from extrarenal losses (GI, drugs, fluids), which have a high (+) urine anion gap
- between the RTAs: remember that Type I & Type II RTA result in hypokelamia, type IV causes hyperkalemia (aldosterone definiciency)
- type I has an low pH (acidotic) urine due to compensatory mechanisms
14
Q
what are the major systemic effects of metabolic acidosis?
A
major ones:
- the cardiac effects:
- cardiac contractility is depressed
- arterial vasodilation –> decreased vascular resistance
others included in chart
15
Q
- what pH defines metabolic alkalosis?
- what other values will likely be seen on a metabolic panel/ABG?
A
- ph > 7.44
- metabolic panel: HCO3 > 28 mmol/L
- ABG: pCO2 > 40 mmHg (usually)
- due to respiratory compensation. metabolic alkalosis induces hypoventilation to retain CO2
