DIT review - Renal 1 Flashcards

1
Q

Describe kidney embryology (pronephros, mesonephros, metanephros)

A
  • Pronephros
    • Degenerates
  • Mesonephros
    • Forms temporary kidney during 1st trimester
    • Later contributes to male genital system
    • Caudal end becomes the ureteric bud which gives risk to ureter, pelvises, calyces, collecting ducts
  • Metanephros
    • Interaction with the ureteric bud induces differentiation and formation of glomerulus through to distal convoluted tubule
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2
Q

What vessel does a horseshoe kidney get stuck under?

A

Inferior mesenteric artery

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3
Q

What are the layers of the glomerular filtration barrier and what layers are responsible for size/charge?

A
  • Fenestrated capillary endothelium
    • Size barrier
  • Basement membrane
    • Negatively charged (contains heparin sulfate) and size barrier
  • Podocyte foot process
    • Visceral layer of Bowman’s capsule
    • Negative charge layer
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4
Q

Describe components and funtion of the juxtaglomerular apparatus

A
  • Decreased MAP -> decreased renal perfusion pressure sensed by macula densa cells of the distal tubule -> activation of juxtaglomerular cells of the afferent arteriole -> conversion of prorenin to renin which is released into the plasma -> renin catalyzes conversion of angiotensinogen to angiotensin I -> in lungs and kidney ACE converts angiotensin I to angiotensin II
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5
Q

What are the 3 stimulators of renin release

A
  • 3 stimulators of renin release
    • Beta-adrenergic stimulation
    • Low Na+ in the DCT
    • Low pressure in the afferent arteriole
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6
Q

Describe the course of the ureters in reference to vas deferens and uterine artery

A

“Water under the bridge”

Ureters pass under the uterine artery or under vas deferens

Retroperitoneal

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7
Q

Describe the fluid composition of the body

A
  • 60-40-20 rule
  • 60% of body mass is water, of that 60%:
    • 40% is ICF
    • 20% is ECF
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8
Q

What is the equation for renal clearance

A
  • C = (U x V) / P
    • C = Clearance
    • U = Urine concentration
    • V = Urine flow rate
    • P = Plasma concentration
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9
Q

What substances are used to estimate GF

A

Inulin and Creatinine

  • Creatinine is freely filtered but not secreted as much as PAH
  • Inulin is freely filtered but not secreted or reabsorbed
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10
Q

What substance is used to estimate renal plasma flow?

A
  • RPF = Blood going to the glomeruli + blood going to the tubules
  • Can be estimated with PAH (PAH is freely filtered and secreted - clearance of PAH > GFR)
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11
Q

What is the formula for filtration fraction and it’s normal value?

A
  • FF = GFR/RPF
  • Normal FF = 20%
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12
Q

Describe the equations for

  • Filtered load
  • Excretion rate
  • Reabsorbed
  • Secretion
A
  • Filtered load
    • Filtered load = GFR x Plasma concentration
  • Excretion rate:
    • Excretion rate = urine concentration x urine flow rate
  • Reabsorbed:
    • Reabsorbed = filtered – excreted
  • Secretion:
    • Secretion = excreted - filtered
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13
Q

When does glucose appear in the urine?

A
  • Glucose is filtered freely and completely reabsorbed in the proximal convoluted tubule by a sodium-dependent glucose transporter up until a saturation point at 375 mg/dL
    • At 160-200 mg/dL some of the nephrons reach max and glucose begins to start appearing in the urine
    • At 350-375 mg/dL, the transporters become fuly saturated and a lot of glucose enters the urine
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14
Q

Describe the rates of absorption in the proximal tubule of:

Na+, Cl-, K+, HCO3-, Urea, Glucose, Inulin, amino acids, creatinine, and PAH

Be able to graph these on a Tubular fluid / plasma filtrate graph

A
  • Anything that falls below the horizontal line (1.0) – more of that soluble is being absorbed relative to water
  • Anything that falls below the horizontal line – less of that solute is being absorbed relative to water
    • The reason that Creatinine and Inulin levels within the tubule are rising is because they are not reabsorbed, but water is, so their relative levels go up
    • PAH is not being reabsorbed and is also being secreted into the tubules
  • Interpretation of graph:
    • PAH is freely filtered and secreted
    • Creatinine is also freely filtered but not secreted as much as PAH
    • Inulin is freely filtered but not secreted or reabsorbed
      • Clearance of Inulin = GFR
    • Urea is freely filtered and poorly reabsorbed
    • Na+ and K+ are reabsorbed at the same rate of water so their concentrations remain constant
    • HCO3- is actively reabsorbed due to carbonic anhydrase
    • Glucose and amino acids are almost 100% reabsorbed in the proximal tubule
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15
Q

What part of the nephron are divalent cations (Mg2+ and Ca2+) reabsorbed and how?

A

Thick ascending limb of loop of Henle

  • Indirectly induces reabsorption of Mg2+ and Ca2+
    • K+ enters the cell from the lumen via NKCC but then leaks back into the lumen, giving the lumen a slight positive charge
    • Cations flow from lumen into cell down the electric gradient
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16
Q

What part of the nephron does PTH work on?

A

Proximal tubule - PTH increases PO4 excretion

Distal convoluted tubule - PTH increases Ca2+ reabsorption

17
Q

Describe the function of the principal vs. intercalated cells of the collecting duct

A
  • Principal cells
    • Reabsorb H2O and Na+
    • Secrete K+
    • ADH acts at V2 receptor on basolateral membrane to stimulate the cell to inset aquaporin channels on apical membrane à increased water reabsorption
  • Intercalated cells
    • Alpha intercalated cells:
      • Secrete H+
      • Reabsorb K+
    • Beta intercalated cells:
      • Secrete HCO3-
18
Q

Describe how you get euvolemic hyponatremia in SIADH

A
  • Increased ADH leads to excessive water retention
  • Body responds to water retention with decreased renin and aldosterone, increased ANP and BNP
    • Causes increase urinary Na+ secretion - Euvolemic hyponatremia
19
Q

Describe the presentation of hypo- and hypernatremia

A
  • Hyponatremia
    • AMS, seizures, stupor, coma
  • Hypernatremia
    • Irritability, stupor, coma
20
Q

Presentation of hyper- and hypocalcemia

A
  • Hypocalcemia
    • Tetany, seizures, QT prolongation, twitching (Chvostek sign), spasm (Trousseau sign)
  • Hypercalcemia
    • Stones, bones, groans, and psychiatric overtones
    • Renal stones, bone pain, abdominal pain, anxiety , AMS, confusion and delirium
21
Q

Presentation of hyper and hypo-kalemia

A
  • Hypokalemia
    • U waves and flattened T waves on ECG, arrhythmias, muscle cramps, spasm, weakness
  • Hyperkalemia
    • Wide QRS and peaked T waves on ECG, arrhythmias, muscle weakness
  • THINK: T-waves match potassium level:
    • High potassium = tall, peaked T wave
    • Low potassium = flat T wave
22
Q

Causes of hyper and hypokalemia

  • otassium (K+)
    • Hypokalemia
      • U waves and flattened T waves on ECG, arrhythmias, muscle cramps, spasm, weakness
      • Causes: high insulin, beta-agonists, alkalosis, cell creation/proliferation, potassium-sparing diuretics, ACE inhibitors
    • Hyperkalemia
      • Wide QRS and peaked T waves on ECG, arrhythmias, muscle weakness
      • Causes: low insulin, beta-blockers, acidosis, Digoxin, cellular lysis
A
    • Hypokalemia
      * Causes: high insulin, beta-agonists, alkalosis, cell creation/proliferation, potassium-sparing diuretics, ACE inhibitors
      • Hyperkalemia
        • Causes: low insulin, beta-blockers, acidosis, Digoxin, cellular lysis
23
Q

Treatment of hyperkalemia

A
  • Treatment: beta-agonist, IV bicarb, IV insulin + dextrose
24
Q

Presentation of hyper- and hypomagnesemia

A
  • Hypomagnesemia
    • Tetany, torsades de pointes, hypokalemia
  • Hypermagnesemia
    • Decreased DTRs, lethargy, bradycardia, hypotension, cardiac arrest, hypocalcemia
25
Q

Describe the defect in type 1 renal tubular acidosis, hyper/hypokalemia, urine pH

A
  • Distal renal tubular acidosis à defect in collecting tubule
  • Alpha-intercalated cells are unable to secrete H+ à acidosis
  • Hypokalemia
  • Urine pH will be > 5.5 (because no H+ in urine)
26
Q

Describe the defect in type 2 renal tubular acidosis, hyper/hypokalemia, urine pH

A
  • Proximal renal tubular acidosis à defect in proximal tubule
  • Impaired HCO3- reabsorption à acidosis
  • Hypokalemia and hypophosphatemia
  • Urine pH < 5.5
27
Q

Describe the defect in type 4 renal tubular acidosis, hyper/hypokalemia, urine pH

A
  • Hyperkalemic renal tubular acidosis
  • Due to hypoaldosteronism -> decreased K+ secretion -> hyperkalemia
  • Hyperkalemia prevents collecting tubules from generating NH4+ -> impaired ammonium excretion
  • Urine pH < 5.5.
28
Q

Causes of respiratory acidosis

A
  • Hypoventilation - airway obstruction, air trapping, lung disease, weak respiratory muscles, opioids
29
Q

Causes of respiratory alkalosis

A
  • Hyperventilation - psychogenic (e.g. anxiety attack), high altitude, acute hypoxemia (e.g. PE), aspirin toxicity
30
Q

Causes of metabolic acidosis

A
  • Anion gap - Adding acid to the blood
    • MUDPILES:
      • M – Methanol
      • U – Uremia (renal failure)
      • D – Diabetic ketoacidosis
      • P – Propylene glycol/Paraldehyde
      • I – Isoniazid/Iron
      • L – Lactic acidosis
      • E – Ethylene glycol (antifreeze)
      • S – Salicylates (aspirin)
  • Non-anion gap - Losing excessive HCO3-
    • Diarrhea, Renal tubular acidosis, Spironolactone, Acetazolamide
31
Q

Cause of metabolic alkalosis

A
  • Losing H+ - excessive vomiting, diuretics, hyperaldosteronism
32
Q

What are normal ABG values (pH, pCO2, pO2, HCO3-)

A
  • pH = 7.35-7.45
  • pCO2 = 35-45
  • pO2 = 75-105
  • HCO3- = 22-28
33
Q

What is Winter’s formula and what does it do?

A
  • Winters formula
    • Predicted respiratory compensation for metabolic acidosis
      • If measured pCO2 > predicted pCO2 – concomitant respiratory acidosis
      • If measure pCO2 < predicted pCO2 – concomitant respiratory alkalosis
    • pCO2 = 1.5(HCO3-) + 8 +/- 2
34
Q
A