Acid-Base Disorders Flashcards
Regarding Henderson Hasselbach equation, what values change and what are the effects in there pH?
-Elevated PCO2 and DECR HCO-3 = decr pH
-Incr HCO-3 and Low PCO2= Incr pH
What 4 things you check in Acid-Base disorders?
-PCO2,pH,HCO-3 and compensation.
What ions are taking in consideration in calculating Anion Gap.
-Na+, HCO-3 and Cl-
Why checking Anion Gap is helpfull in metabolic acidosis?
-To determine where the problem arises. So many types.
Normal value of Anion Gap
PCO2
HCO-3
3-12mEq/L
33-45 mm Hg
22-28 mEq/L
What causes High Anion Gap Metabolic Acidosis?
>12mEq/L of Anion Gap.
-Methanol–>formic acid
Uremia
Diabetic ketoacidosis
Propylene Glycol–>petroleum
Isoniazid and Iron tablets
Lactic acidosis
Ethylene Glycol (Anti-Freeze)
Sialacytes
Normal Anion Gap Metabloc acidosis
Hyperalimentation
Addison dis.–>
Renal Tubular Acidosis
Diarrhea–>loss HCO-3 in stools–>reabsp of Cl-
Acetozolamide
Spironolactone–>incr reabsp HCO-3
Saline infusion 0.9%-> pH=5.5–>body to secrete HCO-3–>acidosis but responds with reabsp. of Cl-
-Same mechanism for every one, when you incr acid in blood–>reabsp more HCO-3 or Cl-
-Loose HCO-3 you reabsp Cl-
To determine respiratory compensation what formula do you use:
Winter Formula
-PCO2= (1.5 x HCO-3+ 8) +/- 2
When is the Winter Formula used
-Metabolic acidosis/alkalosis
Interpret
-PCO2 value within Winter range tells you
-PCO2 value greater than the range of Winter Formula
-PCO2 value less than range of Winter Formula
-metabolic acidosis with appropiate compensatory respiration
-metabolic acidosis + associated respiratory acidosis
-metabolic acidosis + associated respiratory alkalosis
The compensation for respiratory acid-base disorders takes how much?
-At least 24hr. for kidneys to start working.
Respiratory acidosis (>45mmHg)PCO2 ass. with..
Airway obstruction
Sedatives
Acute Chronic Lung dise
Chronic Lung disease
Opiods.
Weakening of resp muscles
-HYPOVENTILATION
Respiratory Alkalosis (<35mmHg) association
Panic attacks
Anxiety attacks
Salicytes
Tumor brains
Pulmunary embolism
Hypoxemia (High altitudes)
HYPERVENTILATION
Metabolic alkalosis 2 causes?
1.Lose of H+–>Hyperaldosteronism + Vomiting
2.HCO-3 gain: Loop diuretics (volume contraction where not much HCO-3 is lossed) + Anta-acids overdose.
Loop diuretics
Anti-acids overdose
Vomiting
Aldosteronism
> 28mmHg HCO-3//pH>7.45
-Compensation..
-Metabolic alkalosis
**-Hypoventilation. **
What happens in compensation for respiratory
-acidosis
-alkalosis
-Reabsp. of HCO-2
-Excretion HCO-3
Diagnosis
A 22-year-old woman presents to her family physician because of increasing fatigue and pale appearance. She reports that her urine appears brown each morning. There is no history of major medical illness. Laboratory studies show RBC of 3 million/mm3 and hemoglobin 10 g/dL.
Which of the following best describes the most likely mechanism of erythrocyte injury in this condition?
-PNH relating respiratory acidosis.
-PIGA gene mutation (hematopoetic stem cells)–>defective CD55 and DAF –>inhibits complememt acting on RBC.At night–>respiratory acidosis–>activate complement an promote hemolytic anemia–>MORNING BLOOD URINE that clears during day.
-Hemolytic anemia (low RBC and Hg), Thrombosis, blood morning urine,-Coomb test
Spironolactone and Diarrhea diffrence in acid-base disorders?
-Both cause Normal Anion Gap Metabolic Acidosis +Decr HC0-3 and incr Cl- and acidic pH.
**Spironolactone has Hyperkalemia **and Diarrhea has Hypokalemia
Hyperchloremic metabolic acidosis, what disorders present like this?
Renal Tubular Acidosis
What RTA leads to this
hypophosphatemic rickets and osteomalacia.
-Type 2 (Faucconi syndrome)
What causes
Contraction metabolic alkalosis?
Vomiting.
-Loose H+ and Volume at same time–>contraction metabolic alkalosis—>RAAS system–>promotes H+ loss in collecting tubules and Increases H+/Na+ exchanger in PCT (excretes H+ and reabsp. Na+)–> reabsp H20 due to the volume loss.
If they give you PCO2 and HCO-3 in acid-base disorder question what should you do?
-Always calculate Winter Formula (compensation)
What is the commonest MIXED acid-base disorder cause by?
-Aspirin cause** metabolic acidosis** (its metabolites–>lactic acid accumulates over time) and respiratory alkalosis by chainging sensitivity towards O2 and CO2–>Hyperventilation.
Effects chronic alcohol users in your acid-base disorders
Furosemide effects on:K+,Cl-,Na+,pH,HCO-3 and compensation
Furosemide causes **renal loss of **sodium, water, and hydrogen ions, sometimes leading to volume depletion, hypokalemia, and metabolic alkalosis with a low urine chloride.
-Incr in PCO2 as compensation.
Benzodiazepines
-Use
A.E
Mechanism related to acid-base disorders
Diazepam,lorazepam
-Incr Cl- channel activity–>incr GABA neuron conduction.
-Used alcohol withdrawl, nigth terrors, sleepwalking, anxiety, panic disorders,status epilepticus.
-A.E: CNS depression severly when used along side Alcohol and Barbituates. //dependence
-Benzodiazepines (eg, lorazepam, diazepam) are administered in the emulsifying agent propylene glycol, and some patients may develop toxicity from this agent. Similar to what happens with ethylene glycol toxicity, this process causes patients to develop hyperosmolarity with an increased osmolar gap (an exogenous osmole) and anion-gap metabolic acidosis due to lactic acidosis.
Barbituates
-Use
A.E
-Phenobarbital,pentobarbital,
-Facilitate GABA action by incr. duration of Cl− channel opening ,thus neuron firing decreases.
-Sedative for anxiety, seizures, insomnia, induction of anesthesia (thiopental).
-Respiratory and cardiovascular depression(can be fatal); CNS depression (can be exacerbated by alcohol use);dependence.
Comparrision between Barbituates vs. Benzodazapines
-Benzo are less sedatives for respiratory depression.
