Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Kidney Lect 13
Acid Base 2
| Question | Answer |
|---|---|
| Can acidosis exist without acidemia? | Acedemia cannot exist without acidosis, but acidosis can exist at any blood pH if more than one disturbance is present; same thing for alkalosis/alkalemia |
| Metabolic disturbance | An acidosis or alkalosis resulting from a primary change in the serum bicarbonate concentration |
| What is the difference between acidosis and acidemia? | Acidosis: pathophysiological process that tends to decrease blood pH; acidemia: arterial blood pH <7.36 |
| What is the difference between alkalosis and alkalemia? | Alkalosis: pathophysiological process that tends to decrease blood pH; alkalemia: arterial blood pH <7.36 |
| Respiratory disturbance | An acidosis or alkalosis resulting from a primary change in the P CO2 |
| Compensation | The physiologic metabolic (renal) and respiratory changes to return the pH toward normal in response to a primary acidosis or alkalosis. |
| Does compensation return pH to normal? | Not completely; time course varies: buffering (minutes to 6 hours), respiratory (minutes to 12 hours), metabolic (24-72 hours) |
| Simple disturbance | A single acid-base process (acidosis or alkalosis) and its expected compensation are present |
| Mixed disturbance | two or more primary acid base disturbances are present. The arterial blood pH will depend on the direction and magnitude of the disturbances |
| What is the primary process and compensation in metabolic acidosis? | Primary process: decreased HCO3-; Compensation: decrease PCO2 |
| What is the primary process and compensation in metabolic alkalosis? | Primary process: increased HCO3-; Compensation: increase PCO2 |
| What is the primary process and compensation in respiratory acidosis? | Primary process: increased PCO2; Compensation: increase [HCO3-] |
| What is the primary process and compensation in respiratory alkalosis? | Primary process: decreased PCO2; Compensation: decreased [HCO3-] |
| Metabolic acidoses are categorized on the basis of ... | the anion that accumulates replacing the bicarbonate ion into hyperchloremic metabolic acidosis and anion-gap metabolic acidosis. |
| anion gap (AG) | defined as the difference between the serum sodium concentration and the sum of the concentrations of the “measured” anions, chloride and bicarbonate. Mathematically, this is represented as: AG = [Na+] – [Cl-] – [HCO 3-] |
| What is a normal anion gap? | 10+/-2 mEq/L ; approximately 2/3 of normal anion gap accounted for by dissociated carboxyl groups on albumin, so adjust in setting of hypoalmbuminemia |
| Describe the changes seen in hypercholermic metabolic acidosis in terms of HCO3-, H+, and Cl- levels | serum bicarb reduced, chloride concentration increases-->NO NET CHANGE IN ANION GAP |
| Describe the changes seen in anion gap metabolic acidosis (aka "delta" acidosis) | decrease in bicarb due to addition of strong acid (e.g. lactic acid)-->AG >20 mEq/L ALWAYS represents a metabolic acidosis, regardless of pH or serum bicarb concentration |
| AG > 20 mEq/L | Always represent metabolic acidosis, regardless of pH or serum bicarbonate concentration |
| What is the easiest way to determine the etiology in a differential diagnosis of metabolic acidosis? | See anion gap; if AG is normal-->hypercholeremic; if AG is increased, High anion gap metabolic acidosis |
| In all the causes of high anion gap metabolic acidosis, you see an excessive production, inegestion, or retention of ____. | strong acid or a compount metabolized into a strong acid |
| What is the differential diagnosis for increased anion gap metabolic acidosis? | diabetic ketoacidosis, alcoholic ketolactic acidosis, lactic acidosis, renal failure, toxins (methanol, ethylene glycol, salicylate, paraldehyde) |
| What is the anion associated with diabetic ketoacidosis? What is the pathophysiology? | In diabetic ketoacidosis, insulin deficiency results in abnormal production of ketoacids: beta hydroxybutyrate, acetoacetate |
| What is the anion associated with alcoholic ketolactic acidosis? What is the pathophysiology? | Fasting after binge drinking leads to low glucose levels, suppressed insulin secretion and ketosis + tissue hypoperfusion and/or liver disease -->increased lactate: beta hydroxybutyrate, acetoacetate, lactate |
| What is the pathophysiology of lactic acidosis? | 1) Increased tissue lactate production (e.g., congenital enzymatic defects, tissue hypoperfusion or hypoxia, enhanced metabolic rate) or 2) decreased lactate utilization (e.g., hypoperfusion, liver disease, ethanol intoxication) |
| Hyperchloremic metabolic acidosis may result from ... | impaired acid excretion, increased bicarbonate losses, or hydrogen ion gain, as outlined below |
| What can lead to impaired renal acid excretion? | Renal failure; distal renal tubular acidosis (classic/hypokalemic [type I], or hyperkalemic [type IV]) |
| What can lead to renal bicarbonate loss? | Proximal renal tubular acidosis (type II), carbonic anhydrase inhibitors, therapy of diabetic ketoacidosis (due to urinary excretion of beta hydroxybutyrate and acetoacetate-->can't regenerate bicarbonate if ketogenesis suppressed) |
| What can lead to GI bicarb loss? | diarrhea, pancreatic drainage, urteral diversion |
| What can lead to acid gain? | Hyperalimentation solutions, ammonium chloride ingestion |
| Proximal renal tubular acidosis (Type II RTA) | characterized by impaired H+ secretion in proximal nephron-->lower bicarb reclaim--> bicarb wasting results when above threshold for reclamation; associated with hypokalemia due to increased distal K secretion (due to hyperaldeosteronism) |
| Proximal RTA in children vs. adults | children: usually due to congenital metabolic defects. adults: usually secondary to acquired proximal tubular damage (e.g. heavy metal exposure, multiple myeloma) |
| Proximal RTA is often accompanied by... | other proximal tubular transport defects including renal glycosuria, phosphate wasting, aminoaciduria and hypouricemia (the Fanconi syndrome). |
| Iatrogenic RTA | may result from therapy with carbonic anhydrase inhibitors (e.g. acetozolamide) |
| Classic distal renal tubular acidosis (Type I RTA) | either from defect in the distal nephron's proton pumps or from back leak of secreted hydrogen ion; urine pH cannot be reduced below 5.5 (daily acid load cannot be excreted) |
| What other electrolyte imbalances can you expect to see with Type I RTA? | may be associated with hypercalciuria and nephrocalcinosis; serum K+ usually low |
| What molecular defects can account for Type I RTA? | Impaired H + -ATPase function Defective bicarbonate/chloride exchanger Defective cytosolic carbonic anhydrase Back-leak of H + ion |
| Hyperkalemic distal renal tubular acidosis (Type IV RTA) | characterized by hyperkalemia and hypercholermic metabolic acidosis, with 2 major patterns of disturbance: aldosterone deficiency/resistance and voltage dependent defect in H+ ion secretion |
| Type IV RTA secondary to aldosterone deficiency/resistance | hyperkalemia primary disturbance, suppressing proximal tubule ammoniagenesis-->metabolic acidosis; urinary acidification is intact; most have mild renal insufficiency |
| Type IV RTA secondary to voltage dependent defect in H+ ion secretion | Primary defect is collecting duct Na+ reabsorption-->decrease in voltage gradient favoring H+ ion secretion-->maximal urinary acidification impaired. Seen in variety of disorders |
| How does metabolic acidosis develop in kidney disease? | Early: patients develop hypercholeremic metabolic acidosis (due to reduced urinary buffers [NH3]); urinary acidification preserved; RAAS axis normal. Chronic: elevated AG due to retention of phosphates, sulfates, and organic anions |
| Urinary anion gap | The urine anion gap (UAG) is calculated as the difference between the measured cations in the urine (Na + and K + ) and urine Cl - : UAG = [Na+] + [K+] – [Cl-] |
| In diarrhea and other non-renal causes of hyperchloremic acidosis, the kidney should be attempting to compensate by increasing ___. The major mechanism for this increase is a marked increase in ___. | net acid excretion; urinary ammonium excretion |
| The UAG will be negative when ___. If there is little ammonium present, the UAG will be ___. | ammonium is present and balanced by negatively charged urinary chloride; zero or positive |
| ____ is the normal respiratory response to metabolic acidosis | Hyperventilation |
| respiratory compensation begins within ___ but takes ____ for maximal response. | minutes; 12-24 hours |
| Winter's formula | P CO2 = 1.5 x [HCO 3- ] + 8 ± 2 |
| In patients with metabolic acidosis, what can you conclude if the PCO2 is greater than predicted with Winter's formula? Less? | Greater-->additional respiratory acidosis; less-->respiratory alkalosis |
| Why is respiratory compensation limited? | respiratory compensation is limited because the P CO2 cannot be lowered much below 10 torr. |
| What is the treatment for metabolic acidosis? | remove underlying cause; alkali replacement required under certain circumstances (if pH less than 7.1 [respiratory compensation maxed and myocardial depression risk]), but only restore to safe range |
| If acute bicarb replacement is indicated, how can you estimate the amount to administer? | HCO 3 - dose (in mmol) = 0.5 x BW (kg) x{[HCO 3 ] desired - [HCO 3 ] actual } |
| How should you treat chronic metabolic acidosis? | Goal: prevent long term sequelae (e.g. bone disease, growth failure, nephrocalcinosis, nephrolithiasis; normalize serum bicarb concentration |
| What are the characteristics of metabolic alkalosis? | high blood pH due to primary elevation in bicarb; accompanied by compensatory increase in PCO2; generation of metabolic alkalosis due to gain of bicarb or loss of acid from body |
| The presence of a sustained metabolic alkalosis implies a defect in what process? | renal bicarbonate excretion; consider etiologies in both generation and maintenance of bicarb levels |
| How can the body lose acid in levels high enough to lead to metabolic alkalosis? | Renal acid loss (diuretic therapy, mineralcorticoid excess, cushing's syndrome, severe potassium depletion, bartter's and gitelman's syndrome, liddle's syndrome) and GI acid loss (gastric acid loss and chloride diarrhea) |
| How can the body gain alkali in levels high enough to lead to metabolic alkalosis? | bicarb administration, milk-alkali syndrome, infusion of organic anions (citrate, acetate, lactate), rapid correction of chronic hypercapnia |
| The maintenance of a metabolic alkalosis requires an impairment ___. | of renal bicarbonate excretion. |
| What (3) things can lead to impaired renal bicarb excretion? | Decreased GFR (decreased effective arterial blood volume [pre-renal state], renal insufficiency), increased proximal tubular bicarb reclaim (pre-renal state, chloride depletion), and increased H+ excretion (mineralocorticoid excess, hypokalemia) |
| How is metabolic alkalosis diagnosed? | Urine chloride concentration (in absence of diuretic): < 20 mmol/L suggests volume depletion while >20 suggests excess mineralocorticoid or Bartter's syndrome. Urine Na+ increase (less reliable) due to increased bicarb loss |
| What is the respiratory compensation for metabolic alkalosis? | Hypoventilation; not as predictale as hyperventilation in metabolic acidosis; hypoventilation limited by hypoxemia, which is a strong respiratory stimulant |
| Saline responsive metabolic alkalosis: treatment | consists of volume expansion with isotonic saline; re-expansion + Cl- restoration-->decrease bicarb resorption distally, trigger bicarbonaturia and lower serum bicarb concentration; if hypokalemic, correct with KCl |
| Metabolic alkalosis due to gastric acid losses, diuretics, chloride depletion and the post-hypercapnic state: treatment | all respond to saline administration |
| Saline resistant metabolic alkalosis: treatment | Patients typically NOT volume or chloride depleted (check serum); may be complicated by mineralocorticoid excess (treat with MR inhibitor) or hypokalemia (give K+ and treat with K+ sparing diuretics if needed) |
| Respiratory acidosis: primary defect and possible causes | primary process is increase in arterial PCO2 due to abnormalities in respiratory function (impaired alveolar gas exchange, obstructive airway disease, disorders of respiratory muscles and chest wall, or CNS inhibition) |
| The renal compensation for respiratory disorders is ___; this is evidence by minimal changes in ___ | slow; minimal increase in serum bicarb |
| In chronic respiratory acidosis, hypercapnia stimulates ___ excretion and leads to an increase in the ___. | renal acid; serum bicarbonate concentration |
| The bicarbonate level generally increases by ___ mmol/L for each 10 torr increase in P CO2 , but rarely rises to greater than 35-40 mmol/L | 3.5 – 5.0 |
| Maximal compensation typically requires ___ hours | (24-) 48 |
| In chronic hypercapnia, what is the major stimulus for ventilation? What can you do this fix this? | hypoxemia; oxygen therapy may inhibit ventilation and worsen hypercapnia-->must be used with extreme caution if chronic respiratory acidosis |
| What are some of the symptoms of acute hypercapnia? | headache, asterixis, confusion, lethargy, obtundation |
| asterixis | flapping tremmor of the hand when it is dorsiflexed; also known as "liver flap" |
| obtundation | dulled or less sharp |
| Respiratory alkalosis: primary process | reduction in arterial PCO2 through hyperventilation |
| What are the most common etiologies for respiratory alkalosis? | hypoxemia, intrapulmonary disease, stimulation of the medullary respiratory center, and mechanical ventilation |
| How are bicarb levels in the serum affected by respiratory alkalosis? How effective is compensation? | Slow; in acute: small decrease in bicarb due to intracell buffering. Chronic: renal bicarb excretion increased and serum bicarb drops by ~5 mmol/L for each 10 torr fall in PCO2 |
| What are signs and symptoms of respiratory alkalosis? | lightheadedness, parasthesias, cramps, carpopedal spasm, seizures (in extreme cases) |
| What is the treatment goal for respiratory alkalosis? | Treat underlying disorder; if related to anxiety, rebreathing into a paper bag may be effective |
| Mixed disturbances | More than one primary acid-base disturbance present (e.g. both metabolic acidosis from diabetic ketoacidosis and respiratory acidosis due to pneumonia); can even be antagonistic (m. acidosis + r. alkalosis) |
| To determine etiology of acid base disorder, what things should you pay attention in history? | Diuretics + vomiting (metabolic alkalosis); diarrhea, alcoholism, or diabetes mellitus (metabolic acidosis); chronic lung disease, CHF, or pneumonia (respiratory acidosis or alkalosis) |
| Kussmaul respirations | slow deep breaths seen as respiratory compensation for metabolic acidosis |
| Fruity oder | seen in ketosis |
| Stigmata of liver disease | respiratory alkalosis |
| volume contraction | metabolic alkalosis |
| CHF | respiratory alkalosis? |
| How do you measure tCO2? | [HCO3-] + [H2CO3] + CO2{serum}; usually, [HCO3-] ~= tCO2 |
| Elevated serum creatinine or hyperglycemia may be associated with... | metabolic acidosis |
| What should you check when analyzing arterial blood gas? | check if pH, PCO2, and [HCO3-] fit simple disturbance; if acidosis, apply Winter's formula to see degree of respiratory compensation; normal pH, PCO2, and [HCO3-] do not exclude acid base disturbance-->check anion gap |
Created by:
karkis77
Popular Physiology sets