FIRST AID 2012 Renal Flashcards

1
Q

What is the course of the ureters?

A

They pass under the uterine artery and under the ductus deferens.

Mneumonic: “Water under the bridge”

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2
Q

What is the 60-40-20 rule?

A

60% total body water
40% ICF
20% ECF

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3
Q

Of our total body weight, how much is water and how much is nonwater?

A

60% total body water

40% nonwater mass

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4
Q

Of the 60% total body water, how much is extracellular fluid and how much is intracellular fluid?

A

1/3 extracellular fluid

2/3 intracellular fluid

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5
Q

Of the extracellular fluid, how much is plasma and how much is interstitial volume?

A

1/4 plasma volume

3/4 interstitial volume

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9
Q

The glomerular filtration barrier is responsible for filtration of plasma according to what two factors?

A
  1. size

2. net charge

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10
Q

What are the 3 things that make up the glomerular filtration barrier?

A
  1. fenestrated capillary endothelium (size barrier)
  2. fused basement membrane with heparin sulfate (negative charge barrier)
  3. epithelial layer consisting of podocyte foot processes
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12
Q

How do you calculate renal clearance?

A

C = (U x V)/ P

U = urine concentration
V = urine flow rate
P = plasma concentration
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13
Q
  1. C = GFR
A
  1. Clearance < GFR = net tubular reabsorption of substance
  2. Clearance >GFR = net tubular secretion of X
  3. Clearance = GFR = no net secretion or reabsorption
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14
Q

What is used to calculate GFR? Why? What is normal GFR?

A

Inulin is used to calculate GFR b/c it is freely filtered and is not reabsorbed or secreted.

Normal GFR is 100 mL/min.

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15
Q

What is another way to write out this equation?

A

GFR = Kf [(Pgc - Pbs) - (TTgc - TTbs)]

GC = glomerular capillary
BS - bowman’s space
TTbs normally equals zero

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16
Q

How do you measure plasma volume?

A

Radiolabeled albumin

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17
Q

How do you measure extracellular volume?

A

Inulin

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18
Q

What is normal osmolarity?

A

290 mOsm

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20
Q

How do you calculate a filtration fraction (FF)? What is considered to be normal FF?

A

FF = GFR / RPF

Normal FF = 20%

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24
Q

What effect will prostaglandins have on the afferent arteriole, RPF, GFR, and FF?

A

Dilate afferent arteriole
Increase RPF
Increase GFR
Constant FF

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25
Q

What effect will ATN II have on the efferent arteriole, RPF, GFR, and FF?

A

Constriction efferent arteriole
Decrease RPF
Increase GFR
Increase FF

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26
Q

Under what situations is the charge barrier of the glomerular filtration barrier lost?

A

In nephrotic syndrome which results in albuminuria, hypoproteinemia, generalized edema, and hyperlididemia

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28
Q

What will happen to RPF, GFR, and FF (GFR/RPF) upon afferent arteriole constriction?

A

Decreased RPF
Decreased GFR
No Change in FF

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29
Q

What will happen to RPF, GFR, and FF upon efferent arteriole constriction?

A

Decreased RPF
Increased GFR
Increased FF

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30
Q

What will happen to RPF, GFR, and FF upon increased plasma protein concentrations?

A

No change in RPF
Decreased GFR
Decreased FF

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31
Q

What will happen to RPF, GFR, and FF upon decreased plasma protein concentrations?

A

No change in RPF
Increased GFR
Increased FF

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32
Q

What will happen to RPF, GFR, and FF upon constriction of the ureter?

A

No change in RPF
Decreased GFR
Decreased FF

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33
Q

What is reabsorbed in the early proximal tubule of the nephron?

A

All of the glucose and amino acids.

Most of the bicarbonate, sodium, chloride, and water.

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38
Q

What is the concentrating segment of the nephron?

A

Thin descending loop of Henle (it passively reabsorbs H2O via medullary hypertonicity b/c it is impermeable to sodium).

Urine becomes hypertonic.

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39
Q

What happens at the thick ascending loop of Henle?

A

Actively reabsorb Na+/K+/Cl- and indirectly induce paracellular reabsorption of Mg2+ and Ca2+.

Unlike the thin descending limb, the thick ascending limb is impermeable to H2O.

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42
Q

What happens at the early distal convolute tubule?

A

Active reabsorption of Na+ and Cl-.

Known as the diluting segment. Makes urine hypotonic.

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46
Q

Can creatinine clearance be used to measure GFR?

A

Yes, but it slightly overestimates GFR b/c creatinine is secreted by renal tubules (inulin isn’t).

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47
Q

Collecting Tubules

A

CAI –> Proximal Tubule
Thiazides –> TAL
Loops –> Distal Convoluted Tubule
K+ sparing diuretics –> Collecting Tubules

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48
Q

What 3 things stimulate the kidneys to secrete Renin?

A
  1. Decreased BP (JG cells)
  2. Decreased Na+ delivery to Macula Densa cells
  3. Increased sympathetic tone (beta-1 receptors)
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49
Q

What can be used to estimate effective renal plasma flow (ERPF)?

A

PAH

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50
Q

Why is PAH clearance used to estimate ERPF?

A

It is both filtered and actively secreted in the proximal tubule. Therefore, this means that all PAH that enters the kidney is excreted.

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52
Q

What are the 6 actions of ATN II?

A
  1. Acts at AT II receptors on VSM –> vasoconstriction –> increase BP
  2. Constrict efferent arterioles –> Increase FF to preserve GFR in low-volume states (ie decreased RBF)
  3. Stimulates the adrenal gland to secrete aldosterone
  4. Stimulates the posterior pituitary to secrete ADH
  5. Increase proximal tubule Na+/H+ activity –> H2O reabsorption
  6. Stimulates hypothalamus –> thirst
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53
Q

How is this equation different from the equation: RBF = RPF (1-Hct)?

A

ERPF underestimates true RPF by ~10%

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56
Q

What are the 4 roles that the kidney plays in endocrine functions?

A
  1. Erythropoietin - released in response to hypoxia from endothelial cells of peritubular capillaries
  2. 1,25-(OH)2 vitamin D - the proximal tubule converts 25-OH vit D to active form 1,25-(OH)2 vit D –> increased intestinal absorption of Ca2+ and phosphate.
  3. Renin - secreted by JG cells in response to decreased renal arterial pressure and increased renal sympathetic discharge (beta1).
  4. Prostaglandins (ie PGE2) - paracrine secretion vasodilates teh afferent arterioles to increase GFR
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57
Q

How does PTH directly and indirectly affect the kidneys on Ca2+ and Phosphate regulation?

A

Directly - acts directly on kidneys to increase renal Ca2+ reabsorption and decrease renal phosphate reabsorption.

Indirectly - stimulates proximal tubule cells to make 1,25 - (OH)2 vit D by stimulating 1alpha-hydroxylase –> increases intestinal absorption of Ca2+ and phosphate.

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58
Q

What is used to estimate GFR?

A

creatinine

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59
Q

What effect does ANP have on the kidney?

A

Secreted in response to increased atrial pressure, it acts on the proximal convoluted tubule by dilating the afferent and constricting the efferent arterioles –> increases GFR and increases Na+ filtration with no compensatory Na+ reabsorption in distal nephron.

Net result: Na+ loss and volume loss

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60
Q

What causes release of PTH?

A
  1. increased plasma phosphate

3. decreased plasma 1,25 (OH)2 vit D

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61
Q

What effect does PTH have on the kidney?

A
  1. At the DCT –> increases Ca2+ reabsorption
  2. At the PCT –> decreases phosphate reabsorption
  3. increases 1,25 (OH)2 vit D production
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62
Q

What can cause hyperkalemia?

A
  1. insulin deficiency (decreased Na/K ATPase)
  2. beta blockers (decreased Na/K ATPase)
  3. acidosis, severe exercise (increased K/H exchanger)
  4. hyperosmolarity
  5. digitalis (blocks Na/K ATPase)
  6. cell lysis
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63
Q

What can cause hypokalemia?

A
  1. insulin (increased Na/K ATPase)
  2. beta agonists (increased Na/K ATPase)
  3. alkalosis (increased K/H exchanger)
  4. hypoosmolarity
64
Q

What is used to estimate RPF?

A

PAH

65
Q

How do you calculate the filtered load?

A

Filtered load = GFR x Plasma concentration

72
Q

What drug will inhibit the effect of prostaglandins on the afferent arteriole?

A

NSAIDS

73
Q

What drug will inhibit the effects of ATN II on the efferent arteriole?

A

ACEI

76
Q

What’s the compensatory response?

A

metabolic acidosis

hyperventilation (immediate)

77
Q

What’s the compensatory response?

A

metabolic alkalosis

hypoventilation (immediate)

78
Q

What’s the compensatory response?

A

respiratory acidosis

increased renal [HCO3-] reabsorption (delayed)

79
Q

What’s the compensatory response?

A

respiratory alkalosis

decreased renal [HCO3-] reabsorption (delayed)

80
Q

What are some causes of respiratory acidosis?

A

Hypoventilation

    1. airway obstruction
    1. acute lung disease
    1. chronic lung disease
    1. opioids, narcotics, sedatives
    1. weakening of respiratory muscles
81
Q

What are some causes of AG metabolic acidosis?

A
Ketoacidosis
Uremia
Salicylate poisoning
Methanol poisoning
Acetaminophen poisoning
Lactic acidosis
Ethylene glycol poisoning

Paraldehyde or Phenformin
Iron tablets or INH

82
Q

What are some causes of normal non-anion gap metabolic acidosis?

A
  1. diarrhea
  2. glue sniffing
  3. renal tubular acidosis
  4. hyperchloremia
83
Q

What are some causes of respiratory alkalosis?

A
  1. Hyperventilation (early high-altitude exposure)

2. Aspirin ingestion (early)

84
Q

What are some causes of metabolic alkalosis with compensation (hypoventilation)?

A
  1. diuretic use
  2. vomiting
  3. antacid use
  4. hyperaldosteronism
85
Q

What is RTA Type 1?

A

Defect in collecting tubule’s ability to excrete H+.

Associated with hypokalemia and risk for calcium-containing kidney stones.

86
Q

What is RTA Type 2?

A

Defect in proximal tubule HCO3- reabsorption.

Associated with hypokalemia and hypophosphatemic rickets.

87
Q

What is RTA Type 4?

A

Hypoaldosteronism or lack of collecting tubule response to aldosterone.

Associated with HYPERKALEMIA and inhibition of ammonium excretion in proximal tubule.
Leads to decreased urine pH due to decreased buffering capacity.

88
Q

RBC casts signify…

A
  1. glomerulonephritis
  2. ischemia
  3. malignant HTN
89
Q

WBC casts signify…

A
  1. tubulointerstitial inflammation
  2. acute pyelonephritis
  3. transplant rejection
91
Q

What does PTH do on the early proximal tubule?

A

Inhibit Na+/Phosphate cotransport –> phosphate excretion.

92
Q

What does ATN II do on the early proximal tubule?

A

Stimulate Na+/H+ exchange –> increase Na+ and H2O reabsorption.

93
Q

Why is the presence of casts so important in hematuria/pyuria?

A

Casts signify that the hematuria/pyuria is of renal origin.

Bladder cancer, kidney stones produce hematuria with NO CASTS.

94
Q

What diseases can cause hematuria but will not create casts in the urine?

A
  1. bladder cancer

2. kidney stones

95
Q

Inhibit Na+/Phosphate cotransport –> phosphate excretion.

A

PTH

96
Q

What diseases are classified under nephritic syndrome?

A
  1. Acute poststreptococcal glomerulonephritis
  2. Rapidly progressive glomerulonephritis
  3. Berger IgA glomerulonephropathy
  4. Alport syndrome
  5. Diffuse proliferative glomerulonephritis
  6. Membrano-proliferative glomerulonephritis
97
Q

What diseases are classified under nephrotic syndrome?

A
  1. Focal segmental glomerulonephritis
  2. Membranous glomerulonephritis
  3. Minimal change disease
  4. Amyloidosis
  5. Diabetic glomerulonephropathy
  6. Diffuse proliferative glomerulonephritis
  7. Membrano-proliferative glomerulonephritis
98
Q

What diseases are classified under both nephritic and nephrotic syndrome?

A
  1. Diffuse proliferative glomerulonephritis

2. Membrano-proliferative glomerulonephritis

99
Q

Stimulate Na+/H+ exchange –> increase Na+ and H2O reabsorption.

A

ATN II

108
Q

Impermeable to Na+

A

Thin descending loop of Henle

111
Q

Impermeable to H2O

A

Thick ascending loop of Henle

115
Q

What does PTH do on the early distal convoluted tubule?

A

Increases Ca2+/Na+ exchange –> Ca2+ reabsorption.

116
Q

What happens at the collecting tubules of the nephron?

A

Reabsorb Na+ in exchange for secreting K+ and H+ (regulated by aldosterone).

117
Q

What does aldosterone do on the collecting tubules?

A

Inserts Na+ channels on luminal side of the principal cell.

118
Q

What does ADH do on the collecting tubules?

A

It binds to V2 receptors to insert aquaporin H2O channels on the luminal side of the principal cell.

136
Q

What cleaves angiotensinogen from the liver into angiotensin I?

A

Renin

137
Q

What cleaves angiotensin I into angiotensin II?

A

ACE

138
Q

Where does ACE come from?

A

Lungs and kidneys

145
Q

What role does ANP play in RAAS?

A

ANP acts as a “check” on RAAS. It relaxes VSM via cGMP –> increase GFR and therefore decrease renin.

148
Q

osmolarity or low blood volume?

A

Low blood volume > osmolarity

149
Q

What is in the juxtaglomerular apparatus?

A

JG cells and macula densa.

159
Q

How can NSAIDs cause acute renal failure?

A

They inhibit the renal production of prostaglandins which are needed to maintain GFR by vasodilating the afferent arterioles.

174
Q

What clinical s/s are seen with low serum [Na+]

A

disorientation, stupor, coma

175
Q

What clinical s/s are seen with high serum [Na+]

A

neurologic: irritability, delirium, coma

176
Q

What clinical s/s are seen with low serum [Cl-]

A

secondary to metabolic alkalosis, hypokalemia, hypovolemia, increased aldosterone

177
Q

What clinical s/s are seen with high serum [Cl-]

A

secondary to non-anion gap acidosis

178
Q

What clinical s/s are seen with low serum [K+]

A

U waves on ECG, flattened T waves, arrhythmias, paralysis

179
Q

What clinical s/s are seen with high serum [K+]

A

Peaked T waves, wide QRS, arrhythmias

180
Q

What clinical s/s are seen with low serum [Ca2]

A

tetany, neuromuscular irritability

181
Q

What clinical s/s are seen with high serum [Ca2+]

A

delirium, renal stones, abdominal pain, not necessarily calciuria

182
Q

What clinical s/s are seen with low serum [Mg2+]

A

neuromuscular irritability, arrhythmias

183
Q

What clinical s/s are seen with high serum [Mg2+]

A

delirium, decreased deep tendon reflexes, cardiopulmonary arrest

184
Q

What clinical s/s are seen with low serum [phosphate]

A

low-mineral ion product causes bone loss, osteomalacia

185
Q

What clinical s/s are seen with high serum [phosphate]

A

high-mineral ion product causes renal stones, metastatic calcifications

268
Q

Granular (“muddy brown”) casts signify…

A
  1. acute tubular necrosis
269
Q

Waxy casts signify…

A
  1. advanced renal disease/CRF
270
Q

Hyaline casts are…

A

nonspecific.

276
Q

What disease can cause pyuria but no casts in the urine?

A
  1. acute cystitis
293
Q

neutrophil-related injury to glomeruli

A

Nephritic syndrome

296
Q

cytokine injury to podocytes; loss of negative charge on GBM

A

Nephrotic syndrome

299
Q

HTN

A

both

302
Q

Pitting Edema

A

both

305
Q

RBC casts and hematuria

A

Nephritic syndrome

308
Q

Massive proteinuria (>3.5 g/day, frothy urine)

A

Nephrotic syndrome