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First Aid > Renal - Physiology > Flashcards

Renal - Physiology Flashcards

1
Q

Fluid compartments

  • Potassium location
  • % of body weight
    • Total body water
    • ICF
    • ECF
  • Plasma volume measured by…
  • Extracellular volume measured by…
  • Osmolarity
A
  • Potassium location
    • HIKIN’: HIgh K INtracellular.
  • 60–40–20 rule (% of body weight):
    • 60% total body water
    • 40% ICF
    • 20% ECF
  • Plasma volume measured by radiolabeled albumin.
  • Extracellular volume measured by inulin.
  • Osmolarity = 290 mOsm/L.
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2
Q

Glomerular filtration barrier

  • Responsible for…
  • Composed of…
  • Pathology of the charge barrier
A
  • Responsible for filtration of plasma according to size and net charge.
  • Composed of…
    • Fenestrated capillary endothelium (size barrier)
    • Fused basement membrane with heparan sulfate (negative charge barrier)
    • Epithelial layer consisting of podocyte foot processes
  • Pathology of the charge barrier
    • The charge barrier is lost in nephrotic syndrome, resulting in albuminuria, hypoproteinemia, generalized edema, and hyperlipidemia.
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3
Q

Renal clearance

  • Cx equation
  • Cx vs. GFR
    • Cx < GFR
    • Cx > GFR
    • Cx = GFR
A
  • Cx = (Ux * V) / Px = volume of plasma from which the substance is completely cleared per unit time.
    • Cx = clearance of X (mL/min).
    • Ux = urine concentration of X (mg/mL).
    • V = urine flow rate (mL/min)
    • Px = plasma concentration of X (mg/mL).
  • Cx vs. GFR
    • Cx < GFR: net tubular reabsorption of X.
    • Cx > GFR: net tubular secretion of X.
    • Cx = GFR: no net secretion or reabsorption.
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4
Q

Glomerular filtration rate

  • Inulin clearance
  • GFR equations
  • Normal vs. reduced GFR
  • Creatinine clearance
A
  • Inulin clearance
    • Can be used to calculate GFR because it is freely filtered and is neither reabsorbed nor secreted.
  • GFR
    • = (Uinulin × V) / Pinulin = Cinulin
    • = Kf [(PGC – PBS) – (πGC – πBS)].
      • GC = glomerular capillary
      • BS = Bowman space
      • πBS normally equals zero.
  • Normal vs. reduced GFR
    • Normal GFR ≈ 100 mL/min.
    • Incremental reductions in GFR define the stages of chronic kidney disease
  • Creatinine clearance
    • An approximate measure of GFR.
    • Slightly overestimates GFR because creatinine is moderately secreted by the renal tubules.
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5
Q

Effective renal plasma flow

  • Effective renal plasma flow (ERPF)
  • ERPF equation
  • RBF equation
A
  • Effective renal plasma flow (ERPF)
    • Can be estimated using para-aminohippuric acid (PAH) clearance because it is both filtered and actively secreted in the proximal tubule.
      • Nearly all PAH entering the kidney is excreted.
    • Underestimates true renal plasma flow (RPF) by ~10%.
  • ERPF = (UPAH × V) / PPAH = CPAH.
  • RBF = RPF / (1 - Hct).
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6
Q

Filtration

  • Equations
    • Filtration fraction (FF)
      • Normal FF
    • Filtered load (mg/min)
  • Estimations
    • GFR
    • RPF
A
  • Equations
    • Filtration fraction (FF) = GFR / RPF.
      • Normal FF = 20%.
    • Filtered load (mg/min) = GFR (mL/min) × plasma concentration (mg/mL)
  • Estimations
    • GFR can be estimated with creatinine clearance.
    • RPF is best estimated with PAH clearance.
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7
Q

Changes in glomerular dynamics

  • For each effect (increased/decreased)
    • RPF
    • GFR
    • FF (GFR / RPF)
  • Afferent arteriole constriction
  • Efferent arteriole constriction
  • Increased plasma protein concentration
  • Decreased plasma protein concentration
  • Constriction of ureter
A
  • Afferent arteriole constriction
    • RPF: Decreased
    • GFR: Decreased
    • FF (GFR / RPF): No effect
  • Efferent arteriole constriction
    • RPF: Decreased
    • GFR: Increased
    • FF (GFR / RPF): Increased
  • Increased plasma protein concentration
    • RPF: No effect
    • GFR: Decreased
    • FF (GFR / RPF): Decreased
  • Decreased plasma protein concentration
    • RPF: No effect
    • GFR: Increased
    • FF (GFR / RPF): Increased
  • Constriction of ureter
    • RPF: No effect
    • GFR: Decreased
    • FF (GFR / RPF): Decreased
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8
Q

Calculation of reabsorption and secretion rate (equations)

  • Filtered load
  • Excretion rate
  • Reabsorption
  • Secretion
A
  • Filtered load = GFR × Px.
  • Excretion rate = V × Ux.
  • Reabsorption = filtered – excreted.
  • Secretion = excreted – filtered.
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9
Q

Glucose clearance

  • Glucose at a normal plasma level
  • At plasma glucose of ~200 mg/dL
  • At plasma glucose of ~375 mg/dL
  • Glucosuria
  • Normal pregnancy
A
  • Glucose at a normal plasma level
    • Completely reabsorbed in proximal tubule by Na+/glucose cotransport.
  • At plasma glucose of ~200 mg/dL
    • Glucosuria begins (threshold).
  • At plasma glucose of ~375 mg/dL
    • All transporters are fully saturated (Tm).
  • Glucosuria
    • An important clinical clue to diabetes mellitus.
  • Normal pregnancy 
    • Decreases reabsorption of glucose and amino acids in the proximal tubule Ž–> glucosuria and aminoaciduria.
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10
Q

Amino acid clearance

  • Reabsorption
  • Hartnup disease
    • Definition
    • Findings
    • Treatment
A
  • Reabsorption
    • Sodium-dependent transporters in proximal tubule reabsorb amino acids.
  • Hartnup disease
    • Definition
      • Autosomal recessive disorder.
      • Deficiency of neutral amino acid (e.g., tryptophan) transporters in proximal renal tubular cells and on enterocytes.
    • Findings
      • Leads to neutral aminoaciduria and decreased absorption from the gut
      • Results in pellagra-like symptoms
    • Treatment
      • Treat with high-protein diet and nicotinic acid.
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11
Q

Nephron physiology:
Early proximal convoluted tubule (PCT)

  • Functions
  • Important hormones
  • % Na+ reabsorbed
A
  • Functions
    • Contains brush border.
    • Reabsorbs all of the glucose and amino acids and most of the HCO3–, Na+, Cl–, PO43–, K+, and H2O.
    • Isotonic absorption.
    • Generates and secretes NH3, which acts as a buffer for secreted H+.
  • Important hormones
    • PTH
      • Inhibits Na+/PO43– cotransport → PO43– excretion.
    • AT II
      • Stimulates Na+/H+ exchange → ↑ Na+, H2O, and HCO3- reabsorption (permitting contraction alkalosis).
  • % Na+ reabsorbed
    • 65–80%
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12
Q

Nephron physiology:
Thin descending loop of Henle

  • Functions
A
  • Functions
    • Passively reabsorbs H2O via medullary hypertonicity (impermeable to Na+).
    • Concentrating segment.
    • Makes urine hypertonic.
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13
Q

Nephron physiology:
Thick ascending loop of Henle

  • Functions
  • % Na+ reabsorbed
A
  • Functions
    • Actively reabsorbs Na+, K+, and Cl-.
    • Indirectly induces the paracellular reabsorption of Mg2+ and Ca2+ through (+) lumen potential generated by K+ backleak.
    • Impermeable to H2O.
    • Makes urine less concentrated as it ascends.
  • % Na+ reabsorbed
    • 10–20%
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14
Q

Nephron physiology:
Early distal convoluted tubule (DCT)

  • Functions
  • Important hormones
  • % Na+ reabsorbed
A
  • Functions
    • Actively reabsorbs Na+, Cl-.
    • Makes urine hypotonic.
  • Important hormones
    • PTH
      • ↑ Ca2+/Na+ exchange → Ca2+ reabsorption.
  • % Na+ reabsorbed
    • 5–10%
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15
Q

Nephron physiology:
Collecting tubule

  • Functions
  • Important hormones
  • % Na+ reabsorbed
A
  • Functions
    • Reabsorbs Na+ in exchange for secreting K+ and H+ (regulated by aldosterone).
  • Important hormones
    • Aldosterone
      • Acts on mineralocorticoid receptorŽ → insertion of Na+ channel on luminal side.
    • ADH
      • Acts at V2 receptor Ž→ insertion of aquaporin H2O channels on luminal side.
  • % Na+ reabsorbed
    • 3–5%
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16
Q

Renal tubular defects

A
  • The kidneys put out FABulous Glittering Liquid:
  • FAnconi syndrome is the 1st defect (PCT)
  • Bartter syndrome is next (thick ascending loop of Henle)
  • Gitelman syndrome is after Bartter (DCT)
  • Liddle syndrome is last (collecting tubule)
17
Q

Fanconi syndrome

  • Type of condition
  • Definition
  • Findings
  • Due to…
A
  • Type of condition
    • Renal tubular defect
  • Definition
    • Reabsorptive defect in PCT.
    • Associated with increased excretion of nearly all amino acids, glucose, HCO3–, and PO43–.
  • Findings
    • May result in metabolic acidosis (proximal renal tubular acidosis).
  • Due to…
    • Hereditary defects (e.g., Wilson disease)
    • Ischemia
    • Nephrotoxins/drugs.
18
Q

Bartter syndrome

  • Type of condition
  • Definition
  • Findings
A
  • Type of condition
    • Renal tubular defect
  • Definition
    • Reabsorptive defect in thick ascending loop of Henle.
    • Autosomal recessive
    • Affects Na+/K+/2Cl– cotransporter.
  • Findings
    • Results in hypokalemia and metabolic alkalosis with hypercalciuria.
19
Q

Gitelman syndrome

  • Type of condition
  • Definition
  • Findings
A
  • Type of condition
    • Renal tubular defect
  • Definition
    • Reabsorptive defect of NaCl in DCT.
    • Autosomal recessive.
    • Less severe than Bartter syndrome.
  • Findings
    • Leads to hypokalemia and metabolic alkalosis, but without hypercalciuria.
20
Q

Liddle syndrome

  • Type of condition
  • Definition
  • Findings
  • Treatment
A
  • Type of condition
    • Renal tubular defect
  • Definition
    • Increased Na+ reabsorption in distal and collecting tubules (increased activity of epithelial Na+ channel).
    • Autosomal dominant.
  • Findings
    • Results in hypertension, hypokalemia, metabolic alkalosis, decreased aldosterone.
  • Treatment
    • Amiloride.
21
Q

Relative concentrations along proximal tubules (529)

  • Tubular inulin
  • Cl- reabsorption
A
  • Tubular inulin 
    • Increased in concentration (but not amount) along the proximal tubule as a result of water reabsorption.
  • Cl- reabsorption
    • Occurs at a slower rate than Na+ in early proximal tubule and then matches the rate of Na+ reabsorption more distally.
    • Thus, its relative concentration increases before it plateaus.
22
Q

Renin-angiotensin-aldosterone system (530)

  • AT II
  • ANP
  • ADH
  • Aldosterone
A
  • AT II
    • Affects baroreceptor function
    • Limits reflex bradycardia, which would normally accompany its pressor effects.
    • Helps maintain blood volume and blood pressure.
  • ANP
    • Released from atria in response to increased volume
    • May act as a “check” on renin-angiotensin-aldosterone system
    • Relaxes vascular smooth muscle via cGMP, causing increased GFR, decreased renin.
  • ADH
    • Primarily regulates osmolarity
    • Also responds to low blood volume states.
  • Aldosterone
    • Primarily regulates ECF Na+ content and volume
    • Responds to low blood volume states.
23
Q

Juxtaglomerular apparatus

  • Consists of…
  • JGA
  • β-blockers
A
  • Consists of…
    • JG cells (modified smooth muscle of afferent arteriole) and the macula densa (NaCl sensor, part of the distal convoluted tubule).
    • JG cells secrete renin in response to decreased renal blood pressure, decreased NaCl delivery to distal tubule, and increased sympathetic tone (β1).
    • Juxta = close by
  • JGA
    • Defends GFR via renin-angiotensin-aldosterone system.
  • β-blockers
    • Can decrease BP by inhibiting β1‑receptors of the JGA, causing decreased renin release.
24
Q

Kidney endocrine functions

  • Erythropoietin
  • 1,25-(OH)2 vitamin D
  • Renin
  • Prostaglandins
A
  • Erythropoietin
    • Released by interstitial cells in the peritubular capillary bed in response to hypoxia.
  • 1,25-(OH)2 vitamin D [image]
    • Proximal tubule cells convert 25-OH vitamin D to 1,25-(OH)2 vitamin D (active form).
  • Renin
    • Secreted by JG cells in response to decreased renal arterial pressure and increased renal sympathetic discharge (β1 effect).
  • Prostaglandins
    • Paracrine secretion vasodilates the afferent arterioles to increase RBF.
    • NSAIDs block renal-protective prostaglandin synthesis –>Ž constriction of the afferent arteriole and decreased GFR
      • This may result in acute renal failure.
25
Q 
Hormones acting on kidney:
Angiotensin II (AT II)
  • Synthesized in response to…
  • Causes…
  • Net effect
A
  • Synthesized in response to…
    • Decreased BP.
  • Causes…
    • Efferent arteriole constriction –> increased GFR and increased FF but with compensatory Na+ reabsorption in proximal and distal nephron.
  • Net effect
    • Preservation of renal function in low-volume state (increased FF) with simultaneous Na+ reabsorption (both proximal and distal) to maintain circulating volume.
26
Q 
Hormones acting on kidney:
Parathyroid hormone (PTH)
  • Secreted in response to…
  • Causes…
A
  • Secreted in response to…
    • Decreased plasma [Ca2+]
    • Increased plasma [PO43–]
    • Decreased plasma 1,25-(OH)2 vitamin D.
  • Causes…
    • Increased [Ca2+] reabsorption (DCT)
    • Decreased [PO43–] reabsorption (PCT)
    • Increased 1,25-(OH)2 vitamin D production (increased Ca2+ and PO43– absorption from gut via vitamin D).
27
Q

Hormones acting on kidney:
Atrial natriuretic peptide (ANP)

  • Secreted in response to…
  • Causes…
  • Net effect
A
  • Secreted in response to…
    • Increased atrial pressure
  • Causes…
    • Increased GFR and increased Na+ filtration with no compensatory Na+ reabsorption in distal nephron.
  • Net effect
    • Na+ loss and volume loss.
28
Q

Hormones acting on kidney:
Aldosterone

  • Secreted in response to…
  • Causes…
A
  • Secreted in response to…
    • Decreased blood volume (via AT II)
    • Increased plasma [K+]
  • Causes…
    • Increased Na+ reabsorption
    • Increased K+ secretion
    • Increased H+ secretion
29
Q

Hormones acting on kidney:
ADH (vasopressin)

  • Secreted in response to…
  • Causes…
A
  • Secreted in response to…
    • Increased plasma osmolarity
    • Decreased blood volume
  • Causes…
    • Binds to receptors on principal cells, causing increased number of water channels and increased H2O reabsorption.
30
Q

Potassium shifts

  • What shift K+ out of the cell
  • What shifting K+ out of the cell causes
  • What shift K+ into the cell
  • What shifting K+ into the cell causes
A
  • What shift K+ out of the cell
    • Patient with hyperkalemia? DO Insulin LAβ work.
    • Digitalis
    • HyperOsmolarity
    • Insulin deficiency
    • Lysis of cells
    • Acidosis
    • β-adrenergic antagonist
  • What shifting K+ out of the cell causes
    • Hyperkalemia
  • What shift K+ into the cell
    • Hypo-osmolarity
    • Insulin (increased Na+/K+ ATPase)
      • Insulin shifts K+ into cells
    • Alkalosis
    • β-adrenergic agonist (increased Na+/K+ ATPase)
  • What shifting K+ into the cell causes
    • Hypokalemia
31
Q

Electrolyte disturbances

  • For each
    • Low serum concentration
    • High serum concentration
  • Na+
  • K+
  • Ca2+
  • Mg2+
  • PO43−
A
  • Na+
    • Low: Nausea and malaise, stupor, coma
    • High: Irritability, stupor, coma
  • K+
    • Low: U waves on ECG, flattened T waves, arrhythmias, muscle weakness
    • High: Wide QRS and peaked T waves on ECG, arrhythmias, muscle weakness
  • Ca2+
    • Low: Tetany, seizures, QT prolongation
    • High: Stones (renal), bones (pain), groans (abdominal pain), psychiatric overtones (anxiety, altered mental status), but not necessarily calciuria
  • Mg2+
    • Low: Tetany, torsades de pointes 
    • High: Decreased DTRs, lethargy, bradycardia, hypotension, cardiac arrest, hypocalcemia
  • PO43−
    • Low: Bone loss, osteomalacia
    • High: Renal stones, metastatic calcifications, hypocalcemia
32
Q

Acid-base physiology

  • For each
    • pH
    • PCO2
    • [HCO3–]
    • Compensatory response
  • Metabolic acidosis
  • Metabolic alkalosis
  • Respiratory acidosis
  • Respiratory alkalosis
A
  • Metabolic acidosis
    • pH: Decreased (compensatory response)
    • PCO2: Decreased (compensatory response)
    • [HCO3–]: Decreased (1º disturbance)
    • Compensatory response: Hyperventilation (immediate)
  • Metabolic alkalosis
    • pH: Increased (compensatory response)
    • PCO2: Increased (compensatory response)
    • [HCO3–]: Increased (1º disturbance)
    • Compensatory response: Hypoventilation (immediate)
  • Respiratory acidosis
    • pH: Decreased (compensatory response)
    • PCO2: Increased (1º disturbance)
    • [HCO3–]: Increased (compensatory response)
    • Compensatory response: Increased renal [HCO3–] reabsorption (delayed)
  • Respiratory alkalosis
    • pH: Increased (compensatory response)
    • PCO2: Decreased (1º disturbance)
    • [HCO3–]: Decreased (compensatory response)
    • Compensatory response: Decreased renal [HCO3–] reabsorption (delayed)
33
Q

Acid-base physiology

  • Henderson-Hasselbalch equation
  • Winters formula
A
  • Henderson-Hasselbalch equation
    • pH = 6.1 + log { [HCO3−] / (0.03 PCO2) }
  • Winters formula
    • The predicted respiratory compensation for a simple metabolic acidosis can be calculated using the Winters formula.
    • If the measured PCO2 differs significantly from the predicted PCO2, then a mixed acid-base disorder is likely present
      • PCO2 = 1.5 [HCO3–] + 8 +/- 2
34
Q

Metabolic/respiratory acidosis/alkalosis & hyperventilation/hypoventilation

  • pH < 7.4
    • PCO2 > 40 mmHg
    • PCO2 < 40 mmHg
  • pH > 7.4
    • PCO2 < 40 mmHg
    • PCO2 > 40 mmHg
A
  • pH < 7.4 = Acidemia
    • PCO2 > 40 mmHg
      • Respiratory acidosis
      • Hypoventilation
    • PCO2 < 40 mmHg
      • Metabolic acidosis with compensation
      • Hyperventilation
      • Check anion gap
  • pH > 7.4 = Alkalemia
    • PCO2 < 40 mmHg
      • Respiratory alkalosis
      • Hyperventilation
    • PCO2 > 40 mmHg
      • Metabolic alkalosis with compensation
      • Hypoventilation
35
Q

Causes of metabolic/respiratory acidosis/alkalosis

  • Respiratory acidosis: Hypoventilation
  • Metabolic acidosis: Check anion gap
  • Respiratory alkalosis: Hyperventilation
  • Metabolic alkalosis with compensation: Hypoventilation
A
  • Respiratory acidosis: Hypoventilation
    • Airway obstruction
    • Acute lung disease
    • Chronic lung disease
    • Opioids, sedatives
    • Weakening of respiratory muscles
  • Metabolic acidosis: Check anion gap
    • Anion gap = Na+ – (Cl- + HCO3-)
    • Increased ​anion gap
      • MUDPILES:
      • Methanol (formic acid)
      • Uremia
      • Diabetic ketoacidosis
      • Propylene glycol
      • Iron tablets or INH
      • Lactic acidosis
      • Ethylene glycol (oxalic acid)
      • Salicylates (late)
    • Normal anion gap (8-12 mEq/L)
      • HARD-ASS:
      • Hyperalimentation
      • Addison disease
      • Renal tubular acidosis
      • Diarrhea
      • Acetazolamide
      • Spironolactone
      • Saline infusion
  • Respiratory alkalosis: Hyperventilation
    • Pulmonary embolism
    • Tumor
    • Salicylates (early)
    • Hypoxemia (e.g., high altitude)
    • Hysteria
  • Metabolic alkalosis with compensation: Hypoventilation
    • Hyperaldosteronism
    • Antacid use
    • Loop diuretics
    • Vomiting
36
Q

Renal tubular acidosis

  • Definition
  • Type 4
    • Defining feature
    • pH
    • Defect
A
  • Definition
    • A disorder of the renal tubules which leads to non-anion gap hyperchloremic metabolic acidosis.
  • Type 4
    • Defining feature
      • Hyperkalemic
    • pH
      • < 5.5
    • Defect
      • Hypoaldosteronism, aldosterone resistance, or K+-sparing diuretics.
      • The resulting hyperkalemia impairs ammoniagenesis in the proximal tubule –> decreased buffering capacity and decreased H+ excretion into urine.
37
Q

Renal tubular acidosis:
Type 1

  • Location
  • pH
  • Defect
  • Assocaited with…
  • Due to…
A
  • Location
    • Distal
  • pH
    • > 5.5
  • Defect
    • Defect in ability of α intercalated cells to secrete H+.
    • Thus, new HCO3- is not generated Ž–> metabolic acidosis.
  • Associated with…
    • Hypokalemia, increased risk for calcium phosphate kidney stones (due to increased urine pH and increased bone turnover).
  • Due to…
    • Amphotericin B toxicity, analgesic nephropathy, multiple myeloma (light chains), and congenital anomalies (obstruction) of the urinary tract.
38
Q

Renal tubular acidosis:
Type 2

  • Location
  • pH
  • Defect
  • Associated with…
  • Due to…
A
  • Location
    • Proximal
  • pH
    • < 5.5
  • Defect
    • Defect in proximal tubule HCO3- reabsorption results in increased excretion of HCO3- in urine and subsequent metabolic acidosis.
    • Urine is acidified by α intercalated cells in collecting tubule.
  • Associated with…
    • Hypokalemia, increased risk for hypophosphatemic rickets.
  • Due to…
    • Fanconi syndrome (e.g., Wilson disease), chemicals toxic to proximal tubule (e.g., lead, aminoglycosides), and carbonic anhydrase inhibitors.

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