DIT review - Renal 1

Question 1

Describe kidney embryology (pronephros, mesonephros, metanephros)

Answer 1

• Pronephros
  
  • Degenerates
• Mesonephros
  
  • Forms temporary kidney during 1^st 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

Question 2

What vessel does a horseshoe kidney get stuck under?

Answer 2

Inferior mesenteric artery

Question 3

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

Answer 3

• 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

Question 4

Describe components and funtion of the juxtaglomerular apparatus

Answer 4

• 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

Question 5

What are the 3 stimulators of renin release

Answer 5

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

Question 6

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

Answer 6

“Water under the bridge”

Ureters pass under the uterine artery or under vas deferens

Retroperitoneal

Question 7

Describe the fluid composition of the body

Answer 7

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

Question 8

What is the equation for renal clearance

Answer 8

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

Question 9

What substances are used to estimate GF

Answer 9

Inulin and Creatinine

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

Question 10

What substance is used to estimate renal plasma flow?

Answer 10

• 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)

Question 11

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

Answer 11

• FF = GFR/RPF
• Normal FF = 20%

Question 12

Describe the equations for

• Filtered load
• Excretion rate
• Reabsorbed
• Secretion

Answer 12

• 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

Question 13

When does glucose appear in the urine?

Answer 13

• 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

Question 14

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

Answer 14

• 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

Question 15

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

Answer 15

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

Question 16

What part of the nephron does PTH work on?

Answer 16

Proximal tubule - PTH increases PO4 excretion

Distal convoluted tubule - PTH increases Ca2+ reabsorption

Question 17

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

Answer 17

• 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-

Question 18

Describe how you get euvolemic hyponatremia in SIADH

Answer 18

• 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

Question 19

Describe the presentation of hypo- and hypernatremia

Answer 19

• Hyponatremia
  
  • AMS, seizures, stupor, coma
• Hypernatremia
  
  • Irritability, stupor, coma

Question 20

Presentation of hyper- and hypocalcemia

Answer 20

• 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

Question 21

Presentation of hyper and hypo-kalemia

Answer 21

• 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

Question 22

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

Answer 22

• • 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

Question 23

Treatment of hyperkalemia

Answer 23

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

Question 24

Presentation of hyper- and hypomagnesemia

Answer 24

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

Question 25

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

Answer 25

* 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)

Question 26

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

Answer 26

* Proximal renal tubular acidosis à defect in proximal tubule * Impaired HCO3- reabsorption à acidosis * Hypokalemia and hypophosphatemia * Urine pH \< 5.5

Question 27

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

Answer 27

* 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.

Question 28

Causes of respiratory acidosis

Answer 28

* Hypoventilation - airway obstruction, air trapping, lung disease, weak respiratory muscles, opioids

Question 29

Causes of respiratory alkalosis

Answer 29

* Hyperventilation - psychogenic (e.g. anxiety attack), high altitude, acute hypoxemia (e.g. PE), aspirin toxicity

Question 30

Causes of metabolic acidosis

Answer 30

* 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

Question 31

Cause of metabolic alkalosis

Answer 31

* Losing H+ - excessive vomiting, diuretics, hyperaldosteronism

Question 32

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

Answer 32

* pH = 7.35-7.45 * pCO2 = 35-45 * pO2 = 75-105 * HCO3- = 22-28

Question 33

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

Answer 33

* 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