Renal Flashcards
New bicarbonate is generated by secretion of protons into urinary buffers (phosphate and ammonia) that are then eliminated. Proton secretion is stimulated by ___________ (2). Bicarbonate reabsorption is stimulated by ____________ (3). The renal response to changes in extracellular pH is slower than the respiratory response, generally requiring ________ hours for a maximal response.
acidosis and aldosterone secretion
hypercapnia, extracellular volume contraction, and severe potassium depletion
24 to 48
For each Type of Stone: Urine pH, type of Crystals, findings on Radiograph: Calcium (oxalate) Uric acid Struvite Cystine
Type of Stone - Urine pH (N 5.5 to 6.0) - Crystals - On Radiograph
Calcium (oxalate) - Increased - dumbbell or envelope - Radiopaque
Uric acid - Decreased - Rhomboid - RadioLUCENT
Struvite - Increased - Coffin lid - Radiopaque (= magnesium ammonium phosphate; more common in women due to assoc with UTIs/urease-prod bacteria such as Proteus)
Cystine - Decreased - Hexagonal - Radiopaque (assoc with cystinuria = inherited defect of AA transport)
Normal serum anion gap
8 to 12 mEq per L
Reclamation of HCO3- is driven by ___________ in the proximal tubule and by ___________ in the distal tubule.
Regeneration of HCO3- occurs mainly in the _________ tubule. This results in the net secretion of hydrogen ion into the tubule, where it combines with _________(2) and is eliminated from the body.
Na/H exchange; the proton pump
distal; phosphate and ammonia
Expected compensation in Metabolic acidosis
1.0 to 1.5 mm Hg fall in PaCO2 for each 1 mEq per L decrease in HCO3- (maximal decrease is to PaCO2 12 to 15 mm Hg)
Expected compensation in Metabolic alkalosis
0.25 to 1.0 mm Hg rise in PaCO2 for each 1 mEq per L rise in HCO3-
Expected compensation in Respiratory acidosis
Acute, 0.1 mEq per L rise in HCO3- for each 1 mm Hg of PaCO2 rise over 40 mm Hg
Chronic, 0.3 mEq per L rise in HCO3- for each 1 mm Hg of PaCO2 rise over 40 mm Hg
Expected compensation in Respiratory alkalosis
Acute, 0.1 to 0.3 mEq per L fall in HCO3- for each 1 mm Hg of PaCO2 decrease below 40 mm Hg
Chronic, 0.2 to 0.5 mEq per L fall in HCO3- for each 1 mm Hg of PaCO2 decrease below 40 mm Hg
Causes of metabolic acidosis With increased anion gap: (4)
Lactic acidosis (from inadequate tissue oxygenation, hepatic failure, neoplasms) Ketoacidosis (from diabetes, starvation, alcoholism) Poisons/drugs (salicylates, methanol, ethylene glycol) Renal failure (chronic, end-stage disease)
Causes of metabolic acidosis With normal anion gap: (3)
Renal tubular disorders (renal tubular acidosis, potassium-sparing diuretics, hypoaldosteronism)
Loss of base (diarrhea, carbonic anhydrase inhibitors, ureterosigmoidoscopy, pancreatic fistula)
Excess acid intake (ammonium chloride, cationic amino acids)
Causes of metabolic alkalosis (4)
Volume loss with chloride depletion (vomiting, gastric drainage, diuretics, villous adenoma) Hypermineralocorticoid states (exogenous steroid treatment, primary aldosteronism, Cushing syndrome, renovascular disease) Severe potassium deficiency Excess alkali intake (milk-alkali syndrome, bicarbonate administration)
Causes of respiratory acidosis (2) and alkalosis (4)
CAUSES OF RESPIRATORY ACIDOSIS
Acute respiratory failure (drug intoxication, cardiopulmonary arrest)
Chronic respiratory failure (chronic obstructive pulmonary disease [COPD], neuromuscular disorders, obesity)
CAUSES OF RESPIRATORY ALKALOSIS
Hypoxia stimulating hyperventilation (asthma, pulmonary edema, pulmonary fibrosis, high altitude, congenital heart disease)
Increased respiratory drive (pulmonary disease, anxiety, salicylate intoxication, cerebral disease, fever)
Cirrhosis, pregnancy
Excessive mechanical ventilation
Sign/symptom in:
- acute metabolic acidosis (1)
- acute respiratory acidosis (1)
- acute respiratory alkalosis (1)
- acute metabolic acidosis: Profound hyperventilation (Kussmaul respiration)
- acute respiratory acidosis: Papilledema with severe, acute hypercapnia
- acute respiratory alkalosis: Neurologic symptoms (paresthesias, numbness, light-headedness)
Technical aspects that can affect the accuracy of ABGs/electrolytes: (5)
- Delay in processing the sample or not keeping the sample on ice
- Contamination of the sample with excess heparin
- Failure to purge air from the syringe
- A difficult arterial puncture leading to a respiratory alkalosis caused by pain and anxiety
- Sampling of venous blood instead of arterial blood: can result in severe misreadings (usually decreased pH and PO2 and increased PCO2), particularly in disease states that impair peripheral oxygen delivery and/or increase peripheral metabolism.
Generally, if the underlying disturbance is corrected, the kidneys and lungs restore acid-base balance; however, several conditions may require specific therapeutic interventions; what are they in each case?
- metabolic acidosis in the setting of chronic renal failure
- severe uncorrectable metabolic acidosis in the setting of acute renal failure
- metabolic alkalosis from volume and chloride loss
- metabolic acidosis in the setting of chronic renal failure (administration of oral bicarbonate)
- severe uncorrectable metabolic acidosis in the setting of acute renal failure (temporary hemodialysis)
- metabolic alkalosis from volume and chloride loss (fluid replacement with saline solution).
The plasma sodium concentration reflects both ________ and ________.
extracellular fluid osmolality and total body water
Treatment of hyponatremia or hypernatremia requires ___________.
assessment of the patient’s volume status
When treating free water deficit in hypernatremia, a maximum of _________ should be replaced in the first _____ hours.
half the water deficit; 24
Potassium levels over 6 may result in which 2 ECG findings? Why must patient be monitored closely?
peaked T waves and diminished R waves
Require close monitoring for cardiac arrhythmias.
Water constitutes approximately _______% of body weight. Approximately ______% of total body water (TBW) is intracellular fluid (ICF), and ________% is extracellular fluid (ECF). The plasma volume constitutes approximately ______% of the ECF, and the remaining ____% is interstitial fluid.
50% to 60%
two thirds; one third
25%; 75%
All principal electrolytes in the body are asymmetrically distributed across cell membranes. ________ is the principal extracellular cation, with _________ and ___________ the main extracellular anions. _____________ (4) are the main intracellular electrolytes.
Sodium, chloride, bicarb
Potassium, calcium, magnesium, and organic anions (e.g., proteins)
____________ generally reflects the osmolality of the ECF.
the plasma sodium concentration (because sodium salts account for more than 90% of the osmolality of the ECF)
Location of peripheral receptors that sense the effective blood volume (3). These receptors regulate renal sodium handling via ________. (2)
atria, central arteries, and juxtaglomerular apparatus
the renin-angiotensin system and a number of natriuretic hormones
Plasma osmolality is regulated via the action of ___________, which is produced in response to _________. What are its actions on the kidney?
antidiuretic hormone (ADH), which is produced by the hypothalamus in response to increased plasma osmolality
ADH acts on the kidney to reduce urine volume and increase urine osmolality, thus conserving water. Similarly, in the absence of ADH, the kidneys produce very dilute urine.
A pure excess of sodium results in _________ (1), as seen in _________ (3).
Edema; heart failure, cirrhosis, and the nephrotic syndrome
Hyponatremia correction in: (1) severe volume depletion, (2) edematous states?
Unless severe neurologic symptoms are present, correction should be at a rate of approximately __________. Care must be taken not to raise the plasma sodium level too rapidly because it can cause _________.
Severe volume depletion: IV normal saline (0.9%) (hypertonic saline is almost never required). Edematous states: free water restriction.
8 to 12 mEq/L/24 hours. neurologic damage (central pontine myelinolysis)
Sustained hypernatremia usually only occurs in which patients?
Hypernatremia results from a deficit in water relative to solute. Hypernatremia invariably results in hyperosmolarity. This in turn normally results in ADH secretion that stimulates renal water conservation and thirst. Therefore, sustained hypernatremia usually only occurs in patients who are unable to respond to thirst by drinking (e.g., young children and mentally and/or physically limited adults).
Hypernatremia correction involves which fluids? How to calculate free water deficit? How quickly should correction be done?
oral or IV replacement of water as well as sodium replacement if required.
FWD = 0.6 × body weight (kg) × ([Na]serum/140) - 1)
Only half of the free water deficit should be replaced in the first 24 hours, and the remainder of the deficit over the next 24 to 48 hours.
___________ is the principal determinant of membrane excitability in nerve and muscle cells.
The ratio of intracellular to extracellular potassium
____________ stimulates renal potassium excretion.
Balance between intracellular and extracellular potassium is influenced by ___________ (2). How does each factor influence this balance?
Aldosterone
(1) Acid-base balance, with acidosis favoring a shift of potassium out of cells. (2) Hormones: Insulin and β-adrenergic catecholamines promote the movement of potassium into cells.
Potassium depletion results from insufficient dietary potassium intake or increased loss. Potassium loss can occur via: (8)
GI loss (diarrhea, vomiting, villous adenoma, ureterosigmoidostomy)
Diuretic use
Metabolic alkalosis (renal wasting because of bicarbonate excess)
Mineralocorticoid excess
Licorice intoxication (caused by a compound with mineralocorticoid-like activity)
Glucocorticoid excess
Renal tubular disease (renal tubular acidosis, certain antibiotics)
Shift of potassium into the intracellular compartment (from insulin effect, alkalosis) can result in hypokalemia without an actual total body potassium deficit
4 tissues/organs where manifestations of hypokalemia are seen; what are the manifestations?
(disturbances in the function of excitable tissues:)
Skeletal muscle (weakness, particularly of the lower extremities; rhabdomyolysis) Smooth muscle (GI ileus) Cardiac muscle (prominent U waves on electrocardiogram; cardiac arrest, with rapid reduction of serum potassium, enhanced digitalis toxicity) Peripheral nerves (decreased or absent tendon reflexes)
Potassium replacement in hypokalemia: what is used in less severe cases? In more severe cases, what are appropriate concentrations and rates of correction?
- generally done via oral supplementation (potassium chloride) - slower and safer
- severe hypokalemia or hypokalemia in patients who cannot absorb oral supplements: IV potassium solutions should normally contain at most 60 mEq per L and should be administered no faster than 20 mEq per hour to avoid cardiac toxicity from transient hyperkalemia.
Hyperkalemia can occur via a number of mechanisms: (6)
Inadequate renal excretion (acute renal failure, end-stage renal failure, tubular disorders)
Adrenal insufficiency
Administration of potassium-sparing diuretics (spironolactone, amiloride)
Tissue damage with release of intracellular potassium (muscle crush injury, hemolysis, internal hemorrhage)
Shift of potassium from the intracellular compartment (acidosis, insulin deficiency, digitalis poisoning, β-adrenergic antagonists)
Excess potassium intake (usually in the setting of underlying renal insufficiency)
Note: in most cases, significant hyperkalemia, regardless of underlying cause, generally has a component of decreased or impaired renal potassium excretion because the kidneys can usually rapidly excrete an excess of potassium present in the serum.
The major toxicity of hyperkalemia is ___________. Electrocardiogram (ECG) manifestations of hyperkalemia include: (6, in order; 2 additional signs)
the development of cardiac arrhythmias
1 Peaking of T waves (earliest sign) 2 Diminished R waves 3 QRS widening 4 PR prolongation 5 Loss of P wave (Atrial asystole) 6 Sine wave
Also:
Complete heart block
Ventricular fibrillation/standstill
Why isn’t the absolute serum potassium level a very good indicator of patients who have a life-threatening potassium overload?
Because the serum potassium represents only a small fraction of the total body potassium load, small changes in serum levels can indicate a significant change in total body potassium. Therefore, the absolute serum potassium level is not a very good indicator of patients who have a life-threatening potassium overload. However, any patient who presents with a potassium level >6.0 mEq per L should be monitored carefully for the development of cardiac arrhythmias.
Tx of hyperkalemia: 3 groups of therapies
Antagonize the toxic effects of excess potassium on excitable membranes (Membrane stabilization): Calcium administration (does not lower plasma potassium levels but counteracts the effect of hyperkalemia on excitable membranes—transient effect)
Immediately lower the serum potassium (Intracellular shift of potassium):
Insulin administration (with concomitant glucose administration to avoid hypoglycemia)
IV bicarbonate
Elimination of excess potassium (slower than the prev 2 groups; use the 1st 2 strategies first in an emergency):
Use of oral potassium-binding resins to promote GI removal of potassium
Diuretics and saline infusion
Dialysis (hemodialysis and peritoneal—generally in several renal impairments)
How do the kidneys regulate blood pressure? (2)
via secretion of renin and prostaglandins
Acute renal failure (ARF) occurs over what time frame?
hours to days
Prerenal ARF etiologies (6 categories):
Hypovolemia (e.g., from blood loss, dehydration)
Decreased cardiac output (e.g., during acute myocardial infarction, cardiac arrest)
Renovascular disease (e.g., dissection of renal artery, renal artery thrombosis)
Systemic vasodilation (e.g., from administration of systemic vasodilator agents)
Renal vasoconstriction (e.g., from administration of vasopressor agents)
Impairment of renal autoregulation of blood flow (e.g., caused by drugs such as angiotensin-converting enzyme [ACE] inhibitors or nonsteroidal anti-inflammatory drugs).
Intrinsic renal ARF etiologies (5):
Vasculitis or microangiopathy
Glomerulonephritis
Acute tubular necrosis (can be caused by an ischemic insult or nephrotoxic drugs such as aminoglycoside antibiotics or radiographic contrast agents)
Interstitial nephritis (often an allergic-type reaction to various drugs such as β-lactam antibiotics)
Tubular obstruction
Postrenal ARF etiologies (3):
Ureteral obstruction (e.g., because of tumor, retroperitoneal hemorrhage, or nephrolithiasis) Bladder neck obstruction (e.g., because of tumor) Urethral obstruction (e.g., secondary to an enlarged prostate, bladder thrombus, or renal calculus)
ARF is more commonly encountered in the hospital setting (occurring in up to ______% of all hospitalized patients), where it is associated with: (6)
5%
Surgery
Trauma (hemorrhage, muscle injury)
Administration of nephrotoxic drugs (aminoglycoside antibiotics, contrast agents)
Bladder catheterization
Sepsis
Shock (low cardiac output states and the use of vasoactive drugs)
Complications and symptoms of ARF commonly seen are: (5)
Intravascular volume overload (dyspnea, orthopnea, edema)
Metabolic acidosis (dyspnea)
Anemia (fatigue)
Hyperkalemia
Uremic syndrome (when BUN is over 60 to 100 mg/dL: anorexia, nausea/vomiting, pruritus, mental status changes, serositis/pericarditis, coagulopathy)
