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Apex > Unit 10 Kidney > Flashcards

Unit 10 Kidney Flashcards

1
Q

The renal cortex contains of what 3 parts of the nephron?

A

Glomeruli
Proximal tubules
Distal tubules

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2
Q

The renal medulla contains of what 2 components of the nephron?

A

Loop of Henle

Collecting ducts

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3
Q

The kidney resides between what levels of the spinal cord?

A

T12 and L2

Right kidney is slightly more caudal to accommodate the liver

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4
Q

What is the point of entry and exit for the renal artery, vein, nerves, lymphatic, and ureters?

A

Hilum

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5
Q

The medulla is divided into several _____.

A

Pyramids

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6
Q

The apex of each pyramid is directed towards the renal pelvis, what is the apex of the pyramid called?

A

Papilla

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7
Q

The papilla contains lots of _______.

A

Collecting ducts

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8
Q

The papilla drain urine into the _____.

A

Minor calyces

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9
Q

Multiple minor calyces converge to form the ______.

A

Major calyces

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10
Q

Multiple major calyces converge to form the ______.

A

Renal pelvis

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11
Q

The renal pelvis empties into the _____.

A

Ureter

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12
Q

What are the calyces, pelvis, and ureters have the capability to do what to help move urine towards the bladder?

A

Contract

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13
Q

List the 6 functions of the kidney

A
  1. Maintenance of extracellular volume and composition
  2. Blood pressure regulation: long and intermediate term
  3. Excretion of toxins and metabolites
  4. Maintenance of acid-base balance
  5. Hormone production
  6. Blood glucose homeostasis
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14
Q

How does the kidney contribute to the volume and composition of the extracellular fluid?

A

There are 2 key hormones that govern how the kidney regulates ECF volume and composition:

  • aldosterone controls ECF volume, sodium and water are reabsorbed together
  • antidiuretic hormone (vasopressin) controls plasma osmolarity, water is reabsorbed but sodium is not
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15
Q

What other solutes besides Na and water does the kidney regulate?

A 
K
Cl
Phos
Mg
H+
Bicarb
Glucose
Urea
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16
Q

How do the kidneys help to regulate BP? What other systems also contribute to the BP regulation?

A

The kidneys provide intermediate no long term BP control:

  • long term control of BP is carried out by the thirst mechanism (intake) and sodium and water excretion (output)
  • Intermediate term control of BP is carried out by the RAAS
  • Short term control of BP is carried out by the baroreceptor reflex
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17
Q

Hoe does the kidney eliminate toxins and metabolites?

A

Glomerular filtration and tubular secretion clear the blood of metabolic byproducts, toxins, and drugs.
Like the liver, the kidney is capable of phase I and II biotransformation

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18
Q

How does the kidney contribute to acid-base balance? Which other organ is essential to this process?

A

The key organs of acid-base balance include the lungs and the kidneys.

  • the lungs excrete volatile acids (CO2) and the kidneys excrete non-volatile acids.
  • the kidneys maintain acid-base balance by titrations hydrogen in the tubular fluid, which creates acidic or basic urine
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19
Q

What stimulates the kidney to release erythropoietin? What does EPO do after it is released?

A

Erythropoietin is released in response to inadequate O2 delivery to the kidney. (Clinical examples: anemia, reduced intravascular volume, hypoxia from altitude, cardiac and/or pulmonary failure)

  • EPO stimulates stem cells in the bone marrow to produce RBCs
  • Severe kidney disease reduces EPO production and leads to chronic anemia
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20
Q

What is calcitriol, and what does it do?

A

Calciferol is synthesized from ingested vitamin D or following exposure to ultraviolet light.

  • in the liver, calciferol is converted to 25 [OH] vitamin D3 (inactive D3)
  • in the kidney (under control of PTH), 25 [OH] vitamin D3 is converted to calcitriol (1,25 [OH]2 vitamin D3, the active form of D3

Calcitriol has 3 functions, it stimulates:

  • the intestine to absorb Ca+2 from food
  • the bone to store Ca+2
  • the kidney to reabsorbed Ca+2 and phosphate
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21
Q

What prostaglandins vasodilate the renal arteries? Which constrict the renal arteries?

A

Vasodilate: PGE2 and PGI2
Constrict: Thromboxane A2

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22
Q

How to the kidneys help blood glucose homeostasis?

A 
They kidneys (like the liver) are capable of synthesizing glucose from amino acids, thereby preventing hypoglycemia during fasting.
The kidneys rival the liver’s ability to perform Gluconeogenesis
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23
Q

How much blood flow do the kidneys receive (% of CO and total flow)

A

20-25% of CO

1000-1250 mL/min

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24
Q

Of the blood delivered to the kidney, how much is filtered at the glomerulus?

A

20%

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25
Q

The filtered volume of blood that enters the tubules is called what?

A

Ultrafiltrate

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26
Q

The other 80% of blood that isn’t filtered in the kidney goes where?

A

It circulates through the peritubular capillaries

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27
Q

After filtration, how much of the ultrafiltrate is reabsorbed into the peritubular capillaries?

A

~99%

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28
Q

What happens to the ultrafiltrate that is not reabsorbed goes where?

A

It is excreted as urine

1-1.5 L/day

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29
Q

All of the blood in the peritubular capillaries eventually goes where?

A

Empties into the inferior vena cava by way of the renal veins

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30
Q

What is the equation for renal blood flow?

A

Renal Blood Flow = (MAP - Renal Venous Pressure) / Renal Vascular Resistance

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31
Q

How much of renal blood flow does the cortex receive? The medulla? What is PO2 in each region?

A

Cortex receives 90% of renal blood flow - PO2 50 mmHg

Medulla and its juxtamedullary nephrons receive 10% of renal blood flow - PO2 10 mmHg

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32
Q

What is the significance of the renal medulla having a lower PO2 than the cortex?

A

Explains why the medulla is more sensitive to ischemia

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33
Q

Renal blood flow decreases ___% per decade of life after age ____.

A

Decreases by 10% per decade of life after age 50

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34
Q

When does renal blood flow reach adult levels?

A

In the neonate, RBF doubles in the first 2 weeks of life and achieves an adult level by 2 years of age

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35
Q

Trace the path of blood through the kidney, starting at the renal artery

A 
Renal artery
Renal segmental arteries 
Interlobar arteries 
Arcuate arteries 
Interlobular arteries 
Afferent arterioles 
Glomerular capillary bed
Efferent arterioles (or filtration)
Peritubular capillary bed
Venules
Interlobular veins
Arcuate veins
Interlobar veins
Renal segmental veins
Renal vein
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36
Q

Discuss the significance of renal autoregulation

A

The purpose of autoregulation is to ensure a constant amount of blood flow is delivered to the kidneys over a wide range of arterial BPs. Glomerular filtration becomes pressure dependent when MAP is outside the range of autoregulation.

  • when renal perfusion is too low, RBF is increased by reducing renal vascular resistance.
  • when renal perfusion is too high, RBF is reduced by increasing renal vascular resistance.
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37
Q

What is the range of RBF for autoregulation?

A

50 - 180 mmHg

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38
Q

Is urine output autoregulated?

A

No. It is linearly related to MAP about 50 mmHg

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39
Q

List the 6 mechanisms that carry out autoregulation. What 2 are the most important?

A
  1. Myotonic mechanism *
  2. Juxtaglomerular apparatus and tubuloglomerular feedback*
  3. Renin-angiotensin-aldosterone system
  4. Prostaglandins
  5. Atrial natriuretic peptide
  6. Sympathetic nervous system
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40
Q

Describe the myogenic mechanism of renal autoregulation

A

If the renal artery pressure is elevated, the myogenic mechanism constricts the afferent arterioles to protect the glomerulus from excessive pressure.
When the renal artery pressure is too low, the myogenic mechanism dilates the afferent arterioles to increase blood flow going to the nephron.

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41
Q

How does tubuloglomerular feedback affect renal autoregulation?

A

The juxtaglomerular apparatus is located in the distal tubule, specifically the region that passes between the afferent and efferent arterioles.
Tubuloglomerular feedback about the sodium and chloride composition in the distal tubule affects arteriolar tone. In turn, this creates a negative feedback loop to maintain renal blood flow.

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42
Q

The kidneys receive sympathetic innervation from what spinal levels?

A

T8 - L1

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43
Q

The SNS innervate s the afferent and efferent arterioles, what, if any, is the significance of this?

A

Under normal conditions the internal auto regulatory mechanisms override the external effects of the SNS, but in times of stress or when exogenous catecholamines are administered, the SNS cause reduce RBF.

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44
Q

How does the surgical stress response affect RBF?

A

The surgical stress response induces a transient state of vasoconstriction and sodium retention. This persists for several days, resulting in oliguria and edema. Vasoconstriction of the renal vasculature during this time predisposes the kidneys to ischemic injury and nephrotoxicity from drugs administered during the perioperative period.

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45
Q

What does the juxtaglomerular apparatus monitor? Where is it located?

A

Monitors renal perfusion and solute concentrate

Located in the distal tubule, specifically the region that passes between the afferent and efferent arterioles

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46
Q

What does the juxtaglomerular apparatus monitor in the distal tubule? What effect does this carry out?

A

Tubuloglomerular feedback about the sodium and chloride composition in the distal tubule affects arteriolar tone. In turn, this creates a negative feedback loop that adjusts renal vascular resistance and renin secretion in an effort to maintain RBF.

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47
Q

What 3 conditions increase renin release?

A
  1. Decreased renal perfusion pressure
  2. SNS activation
  3. Tubuloglomerular feedback
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48
Q

List 6 causes of decreased renal perfusion pressure than leads to increased renin release

A 
Hemorrhage
PEEP
CHF
Liver failure with ascites
Sepsis
Diuresis
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49
Q

List 2 causes of SNS activation that lead to increase renin release

A

Beta 1 stimulation via:
Circulating catecholamines
Exogenous catecholamines

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50
Q

How does the tubuloglomerular feedback mechanism increase renin release?

A

The macula densa in the distal tubule contains chemoreceptors that monitor Na and Cl in the tubular fluid, when there is decreased sodium and chloride in the distal tubule renin release is increased

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51
Q

List the steps involved in the renin angiotensin aldosterone pathway

A

Decreased renal perfusion/ SNS activation/ Tubuloglomerular feedback
Renin release (from juxtaglomerular cells)
Converts angiotensinogen into angiotensin I
Ace from the lungs converts angiotensin I into angiotensin II
Angiotensin II leads to:
Vasoconstriction of the peripheral vessels
Vasoconstriction of the efferent arteriole
Aldosterone release from the adrenal gland
ADH release from the posterior pituitary
Na+ reabsorption in the proximal tubule
Thirst

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52
Q

Where is aldosterone produced, and what is its function?

A

Aldosterone is a steroid hormone that is produced in the zone glomerulosa of the adrenal gland.
By stimulating the Na/K-ATPase in the principal cells of the distal tubules and collecting ducts, aldosterone causes:
Na+ reabsorption
Water reabsorption
K+ excretion
The net effect of aldosterone increases blood volume but does not affect osmolarity. This is because the water follows sodium in direct proportions when it’s reabsorbed into the peritubular capillaries.

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53
Q

In addition to RAAS stimulation, aldosterone relapse is increased by what 2 things?

A

Hyperkalemia

Hyponatremia

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54
Q

List 2 disorders of aldosterone release

A

Conn’s disease occurs with excess aldosterone production. It causes sodium retention and potassium loss.
Inadequate aldosterone produced ion in isolation is uncommon. Addison’s disease is usually the result of adrenocortical insufficiency (destruction of all of the cortical zones).

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55
Q

Where is antidiuretic hormone produced, and what is its function?

A

ADH is produced in the supraoptic and paraventricular nuclei of the hypothalamus. It is released from the posterior pituitary gland in response to:

  • increased osmolarity of the ECF
  • Decreased blood volume
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56
Q

What does osmolality measure?

A

Number of osmoles per kilogram of solvent

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57
Q

What does osmolarity measure?

A

Number of osmoles per liter of solvent

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58
Q

What is the principal determinant of osmolarity? What else is it affected by?

A

Sodium concentration*
Glucose
Blood urea nitrogen

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59
Q

What is the equation for serum osmolarity? What is the normal osmolarity?

A

Serum osmolarity = 2[Na] + (GLU/18) + (BUN/2.8)

Normal osmolarity = 280 - 290 mOsm/L

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60
Q

How does increased osmolarity of the ECF cause ADH release?

A

An increased ECF sodium concentration shrinks the osmoreceptors in the hypothalamus. This initiates the process of transporting ADH from the hypothalamus to the posterior pituitary gland. After this, ADH is released into the systemic circulation.
The thirst reflex is activated and antidiuresis prevents additional water loss. As the kidneys conserve water, the urine becomes more concentrated (osmolarity increases)

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61
Q

How does decreased blood volume lead to ADH release?

A

When blood volume declines, unloading of the baroreceptors in the carotid bodies, transverse aortic arch, great veins, and right atrium stimulate ADH release

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62
Q

How does ADH restore BP?

A
  1. ADH stimulates the V2 receptor in the collecting ducts (increases cAMP)
    - under the direction of ADH, aquaporin-2 channels (water channels) are inserted into the walls of the collecting ducts
    - this facilitates water reabsorption, reduces plasma osmolarity, and increases urine osmolarity
    - the net result is an expansion of the plasma volume
  2. ADH stimulates the V1 receptor and causes vasoconstriction in the peripheral vasculature (increase IP3, DAG, Ca+)
    - the net result is an increased SVR
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63
Q

What is the half life of ADH?

A

5 - 15 minutes

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64
Q

What clinical situations increase ADH release?

A 
While anesthetic agents to do directly affect ADH homeostasis, they do impact arterial blood pressure and venous blood volume. In turn, these changes increase ADH release:
PEEP
PPV
HoTN
Hemorrhage
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65
Q

List 3 mechanisms that promote renal vasodilation

A
  1. Prostaglandins (inhibited by NSAIDs)
  2. Atrial natriuretic peptide (increased RAP -> Na+ and water excretion)
  3. Dopamine-1 receptor stimulation (increased RBF)
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66
Q

What affect on RAAS do the 3 pathways that promote renal vasodilation have?

A

Renal vasodilation antagonizes the effects of RAAS on renal blood flow

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67
Q

Compare and contrast the location and function of dopamine 1- and 2 receptors.

A

DA1 receptors:
Location - renal vasculature, tubules
2nd messenger - increased cAMP
Function - vasodilation, increased RBF, increased GFR, diuresis, sodium excretion

DA2 receptors:
Location - presynaptic SNS nerve terminal
2nd messenger - decreased cAMP
Function - decreased NE release

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68
Q

Does dopamine improve outcome in acute kidney injury?

A

No. While dopamine increases UOP, there is no solid evidence to support that renal dose dopamine either prevents or treats AKI.

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69
Q

What is the mechanism of action of fenoldapam? Why is it used?

A

A selective DA1 receptor agonist that increases RBF.
Low dose fenoldopam 0.1 - 0.2 mcg/kg/min is a renal vasodilator and increases RBF, GFR, and facilitates Na+ excretion without affecting arterial BP.
It may offer renal protection during aortic surgery and during CPB.
Fenoldopam reduces the requirement for dialysis and in-hospital mortality in cardiac surgery patients.

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70
Q

How much of the renal blood flow is filtered at the glomerulus? Where does the rest go?

A

Renal blood flow = 1000 - 1250 mL/min
Glomerular filtration rate = 125 mL/min or 180 L/day or ~20% of RBF

The filtration fraction is 20%, this means that 20% of the RBF is filtered by the glomerulus and 80% is delivered to the peritubular capillaries

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71
Q

What is freely filtered by the glomerulus? (3)

A

Water
Electrolytes
Glucose

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72
Q

What prevents proteins from entering the glomerular filtrate?

A

The basement membrane of the glomerulus has a negative charge
Albumin has a negative charge

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73
Q

Glomerular filtrate is identical to the plasma except that it does not contain what? (3)

A

Plasma proteins
RBCs
WBCs

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74
Q

Kidney disease results in destruction of the basement membrane, which allows what to occur?

A

Filtration of proteins into the tubules -> proteinuria

75
Q

What determines GFR?

A

Hydrostatic pressure across the glomerulus

76
Q

What are the 3 determinants of glomerular hydrostatic pressure? How do each affect GFR?

A

Arterial blood pressure:
-increased MAP increases GFR and decreased MAP decrease GFR
-autoregulation safeguards against hypo- and hypertension
Afferent arteriole resistance:
-constriction of the afferent arteriole reduces GFR
-dilation of the afferent arteriole increases GFR
Efferent arteriole resistance:
-mild constriction reduces flow towards the peritubular capillaries and increases GFR
-excessive constriction reduces RBF and GFR
-dilation increase flow towards the peritubular capillaries and reduces GFR

77
Q

How do changes in afferent arteriole diameter, efferent arteriole diameter, and plasma protein concentration affect net filtration pressure?

A

Constriction of afferent arteriole: decrease RBF, decrease GFR, no change in filtration fraction.
Constriction of efferent arteriole: decrease in RBF, increase in GFR, increase in filtration fraction.
Increased plasma protein: no change in RBF, decrease in GFR, decrease in filtration fraction.
Decreased plasma protein: no change in RBF, increase in GFR, increase in filtration fraction.

78
Q

Define reabsorption, secretion, and excretion

A

Reabsorption: substance is transferred from the tubule to the peritubular capillaries
Secretion: substance is transferred from the peritubular capillaries to the tubules
Excretion: substance is removed from the body in the urine

79
Q

Describe the fate of sodium at each location in the nephron

A 
Proximal tubule 65% sodium reabsorption 
Loop of Henle thick ascending limb 20% sodium reabsorption 
Distal tubule 5% sodium reabsorption 
Collecting duct 5% sodium reabsorption 
Urine 5%
80
Q

Reabsorption of water occurs by osmosis, what about reabsorption of electrolytes?

A

Requires energy, ATP

81
Q

What are the key functions of each part of the nephron?

A 
Proximal tubule:
-bulk reabsorption of solutes
-bulk reabsorption of water
Loop of Henle (descending):
-countercurrent mechanism
-highly permeable to H2O
Loop of Henle (ascending):
-countercurrent mechanism (concentrates urine)
-no permeability to H2O
Distal tubule:
-Fine tunes solute concentration (aldosterone and ADH)
Collecting duct:
-regulates final concentration of urine (aldosterone and ADH)
82
Q

Describe the mechanism of action, clinical use, and key side effects of carbonic anhydrase inhibitors.

A

Acetazolamide and Dorzolamide
MOA: noncompetative inhibition of carbonic anhydrase in the proximal tubule -> net loss of HCO3- and Na+ with a net gain on H+ and Cl-
Clinical uses: open angle glaucoma, altitude sickness, central sleep apnea syndrome
Key side effects: metabolic acidosis, hypokalemia, with COPD loss of bicarb ions in the urine (reduced buffer) may exacerbate CNS depression from hypercarbia

83
Q

Describe the mechanisms of action, clinical use, and key side effects of osmotic diuretics.

A

Mannitol, Glycerin, and Isosorbide
MOA: osmotic diuretics are sugars that undergo filtration but not reabsorption. They inhibit water reabsorption in the proximal tubule (primary site) as well as the loop of Henle. Water is excreted in excess of electrolytes.
Clinical uses: free radical scavenging, prevention of AKI (little evidence of support), intracranial HTN
Key side effects: volume overload in CHF patients, pulmonary edema, if BBB is disrupted mannitol will enter the brain and cause cerebral edema

84
Q

Describe the mechanisms of action, clinical use, and key side effects of loop diuretics.

A

Furosemide, bumetanide, ethacrynic acid
MOA: loop diuretics poison the Na-K-2Cl transporter in the medullary region of the thick portion of the ascending loop of Henle (primary site). The amount of sodium that remains in the tubule overwhelms the distal tubule’s reabsorption capability. Thus, a large volume of dilute urine is excreted. K, Ca, Mg, and Cl are lost to urine as well.
Clinical uses: HTN, CHF/acute pulmonary edema, hypercalcemia
Key side effects: Hypokalemic hypochloremic metabolic alkalosis, hypocalcemia, hypomagnesemia, hypovolemia, ototoxicity (ethacrynic acid > furosemide), reduced lithium clearance

85
Q

Describe the mechanisms of action, clinical use, and key side effects of thiazide diuretics

A

Hydrochlorothiazide, metolazone, indapamide
MOA: thiazides inhibit the Na-Cl transporter in the distal tubule
Clinical uses: HTN, CHF, osteoporosis (reduces Ca+ excretion), nephrogenic diabetes insipidus
Key side effects: hyperglycemia, hypercalcemia, hyperuricemia (caution with gouty arthritis), hypokalemic hypochloremic metabolic alkalosis, hypovolemia

86
Q

Describe the mechanisms of action, clinical use, and key side effects of potassium-sparing diuretics

A

Spironolactone, amiloride, triamterene
MOA: amiloride and triamterene inhibit K secretion and Na reabsorption in the collecting ducts. Their function is independent of aldosterone. Spironolactone exists in a subclass of K-sparing diuretics called aldosterone antagonists. By blocking aldosterone at mineralocorticoid receptors, it inhibits K secretion and Na reabsorption in the collecting ducts.
Clinical uses: reduce K loss in a patient receiving loop or thaizide diuretics, secondary HTN
Key side effects: hyperkalemia (risk increased with concurrent NSAIDs, BB, or ACEI), metabolic acidosis, gynecomastia, libido changes (spironolactone), nephrolithiasis (triamterene)

87
Q

List 3 tests of GFR and give the normal values for each

A

Glomerular function is measured by GRF
Blood urea nitrogen 10 - 20 mg/dL
Serum creatinine 0.7 - 1.5 mg/dL
Creatinine clearance 110 - 150 mL/min

88
Q

List 4 tests of tubular function and give the normal values for each

A

Tubular function is measured by urine concentrating ability
Fractional excretion of Na+ 1 - 3%
Urine osmolality 65 - 1400 mOsm/L
Urine sodium concentration 130 - 260 mEq/day
Urine specific gravity 1.003 - 1.030

89
Q

What is urea? What is included in a differential diagnosis of a low BUN? How about a high BUN?

A

Urea is the primary metabolite of protein metabolism in the liver (amino acids -> ammonia -> urea).
Because it undergoes filtration AND reabsorption, it is a better indicator of uremic symptoms that as a measurement of GFR
BUN <8 mg/dL: overhydration, decrease urea production (malnutrition, severe liver disease)
BUN 20-40 mg/dL: dehydration, increased protein input (high protein diet, GI bleed, hematoma breakdown), catabolism (trauma, sepsis), decreased GFR
BUN >50 mg/dL: decreased GFR

90
Q

What is creatinine?

A

Creatine is produced by skeletal muscle, and creatinine is a metabolic byproduct of creatine breakdown.
Creatinine production is constant and is directly proportion to muscle mass.
It undergoes renal filtration but not reabsorption, this makes is a good indicator of GFR.
A 100% increase in creatinine indicates a 50% reduction in GFR.

91
Q

What is BUN:Creatinine ration? What do the numbers mean?

A

Since BUN undergoes filtration and reabsorption and creatinine undergoes filtration but no reabsorption, the ratio of these substances in the blood can help us evaluate the state of hydration.
The normal ratio is 10:1
A BUN:Creatinine of >20:1 suggests prerenal azotemia
Non-renal causes of elevated BUN can also affect this ratio

92
Q

What test is the best indicator of GFR? How is this value calculated?

A

Creatinine clearance is the most useful indicator of GFR

GFR = [(140 - age) x kg] / [72 x serum Cr (mg/dL)]

In women this value should be multiplied by 0.85 to account for a smaller muscle mass

93
Q

How do you interpret the fraction excretion of sodium?

A

Fe(Na+) relates sodium clearance to creatinine clearance

  • if Fe(Na+) <1% then more sodium is conserved relative to the amount of creatinine cleared, this suggests prerenal azotemia.
  • if Fe(Na+) >3% then more sodium is excreted relative to the amount of creatinine cleared, this suggests impaired tubular function.
94
Q

Urinary sodium, working kidneys vs failing kidneys

A

Working kidneys are able to conserve sodium, while failing kidneys waste sodium

95
Q

Large amounts of protein in the urine indicate what?

A

Glomerular injury >750 mg/day or 3+ or more by urinalysis

96
Q

What is specific gravity?

A

Assesses the weight of urine relative to sterile water
It measures the kidney’s ability to concentrate or dilute urine
Higher # = more concentrated urine (more solutes)
Lower # = less concentrated urine (less solutes)

97
Q

What is a better best of tubular function, specific gravity or urine osmolality?

A

Urine osmolality

98
Q 
Prerenal oliguria:
Fractional excretion of Na+
Urinary Na+
Urine osmolality
BUN:Creatinine ratio
Sediment
A 
Fractional excretion of Na+ : < 1%
Urinary Na+ : <20 mEq/L
Urine osmolality: >500 mOsm/kg
BUN:Creatinine ratio: > 20:1
Sediment: normal, possible hyaline casts
99
Q 
Acute tubular necrosis:
Fractional excretion of Na+
Urinary Na+
Urine osmolality
BUN:Creatinine ratio
Sediment
A 
Fractional excretion of Na+ : >3
Urinary Na+ : >20
Urine osmolality: <400
BUN:Creatinine ratio: 10 - 20:1
Sediment: tubular epithelial cells, granular casts
100
Q

What is the most common cause of perioperative AKI? Who is at the highest risk?

A

Ischemia-reperfusion injury

Pre-existing kidney dz
Prolonged renal hypoperfusion
CHF
Advanced age
Sepsis
Jaundice
High risk surgery (use of aortic cross clamp and liver transplant)
101
Q

What are the 2 modern methods used to classify the severity of renal injury?

A

RIFLE Criteria: risk, injury, failure, loss, end-stage kidney disease
Acute Kidney Injury Network: AKIN

102
Q

Both RIFLE and AKIN grade renal function on what 2 things?

A

Serum creatinine and urinary output

  • serum creatinine is a more sensitive indicator or renal dysfunction
  • both methods highlighted that kidney injury occurs along a continuum
103
Q

What is the problem with using urine output as a surrogate of renal perfusion?

A

Oliguria is often the result of the physiologic response to stress

104
Q

RIFLE:

R-risk criteria

A

Increased Cr 50%
Or
Decreased GFR > 25%

UOP < 0.5 mL/kg/hr x 6 hr

105
Q

RIFLE:

I-injury criteria

A

Increased Cr 100%
Or
Decreased GFR > 50%

UOP <0.5 mL/kg/hr x 12 hr

106
Q

RIFLE:

F-failure criteria

A 
Increased Cr 200%
Or
Decreased GFR > 75%
Or
Serum Cr of 4 mg/dL or more (with acute rise of 0.5 mg/dL)

UOP <0.3 mg/kg/hr x 24 hr
Or
Anuria x 12 hr

107
Q

RIFLE:

L- loss criteria

A

Complete loss of renal function > 4 weeks

Requires renal replacement therapy

108
Q

RIFLE:

E- ESKD criteria

A

Complete loss of renal function > 3 months

Requires renal replacement therapy

109
Q

AKIN:

Stage I criteria

A

Increased Cr 50%
Or
0.3 mg/dL

UOP <0.5 mg/kg/hr x 6 hr

110
Q

AKIN:

Stage II criteria

A

Increased Cr 100%

UOP <0.5 mg/kg/hr x 12 hr

111
Q

AKIN:

Stage III criteria

A

Increased Cr 200%
Or
Cr 4 mg/dL or more (with acute rise of 0.5 mg/dL)

UOP <0.3 mg/kg/hr x 24 hr
Or
Anuria x 12 hr

112
Q

What is the most common cause of prerenal injury? What is the treatment?

A

Hypoperfusion: perfusion is impaired as a result of hypovolemia, decreased CO, systemic vasodilation, renal vasoconstriction, or increased intra-ABD pressure. There is no intrinsic damage, yet.

Treatment:
Reduce risk of prerenal azotemia by maintaining MAP >65 mmHg and providing appropriate hydration.
Restoration of RBF with IVF, hemodynamic support, and/or pRBCs
Renal prostaglandins mediate vasodilation in the kidney. NSAIDs reduce prostaglandin synthesis, avoid them if prerenal injury is a concern.
An improvement in UOP following an IVF bolus confirms the diagnosis of prerenal injury

113
Q

What is intrinsic renal injury? What is the treatment?

A

Intrinsic injury: parenchymal
While intrinsic injury can be caused by injury to the tubules, glomerulus, or the interstitial space, focus on acute tubular necrosis.
ATN is usually caused by ischemia or nephrotoxic drugs.
-medulla is more susceptible to ischemia
-nephrotoxic drugs: contrast, nephrotoxic ABX, NSAIDs
Treatment: restore renal perfusion, supportive

114
Q

What is post renal injury? What is the treatment?

A

The result of an obstructive phenomena, occurring anywhere between the collecting system and the urethra.
Treatment: relieve obstruction

115
Q

Concepts of prerenal injury:

A 
Intravascular volume depletion
Decreased CO
Systemic Vasodilation 
Renal vasoconstriction
Increased abdominal pressure
116
Q

Concepts for intrinsic renal injury:

A

Tubular injury
Tubulointerstitial injury
Glomerular injury
Renal Vasculature Large Vessels

117
Q

Concepts for postrenal injury:

A

Urinary tract obstruction

118
Q

The risk of prerenal azotemia is reduced by what 2 things?

A

maintaining MAP of > 65

Appropriate hydration

119
Q

What is the deal with hydroxyelthyl starches?

A

They are associated with an increased risk of renal morbidity.
While there is no clear benefit between crystal loads and colloids

120
Q

What can occur with excessive use of 0.9% NaCl?

A

Hyperchloremic metabolic acidosis

121
Q

The attempt to convert oliguria to non oliguria AKI with the use of diuretics increases the risk of what?

A

Additional renal injury as well as mortality

122
Q

What can occur in health patients with alpha-1 agonists?

A

They can reduce renal blood flow

123
Q

In septic patients why is the use of alpha-1 agonists beneficial?

A

As long as MAP is supported, the benefits of increased renal perfusion outweigh the renal vasoconstrictive effects

124
Q

What does vasopressin preferentially constrict?

A

The efferent arteriole, it maintains GFR and UOP better than norepinephrine or phenylephrine

125
Q

What are the first and second most common causes of chronic kidney disease?

A

Most common: diabetes mellitus

Second most common: hypertension

126
Q

Define the 5 stages of chronic kidney disease

A 
Stage 1: normal : GFR 90 or more
Stage 2: mildly decreased: GFR 60-89
Stage 3: moderately decreased: GFR 30-59
Stage 4: severely decreased: GFR 15-29
Stage 5: kidney failure: 15 or less
127
Q

S/Sx of uremic syndrome (5)

A 
anemia
Fatigue
N/V
Anorexia
Coagulopathy
128
Q

How does uremia affect coagulation? What is the most accurate predictor of bleeding risk?

A

Uremic patients are at increased risk of bleeding.
-bleeding time is a measure of platelet function. It is elevated by uremia and is the most accurate predictor of bleeding risk

129
Q

How are PT, PTT and platelet count affected with uremia?

A

They are normal

130
Q

What is the first line treatment for uremia? What else may be used?

A

Desmopressin (von WIllebrand factor VIII).
Cryoprecipitate may be used to provide VIII-vWF, however its use is associated with an increased risk of viral transmission.
Dialysis improves bleeding time, so it should be performed within 24 hours of surgery.

131
Q

Why are patients with chronic kidney disease often anemic? What is the treatment for this?

A

Decreased erythropoietin production leads to a normochromic anemia.
Excess parathyroid hormone also contributes to anemia by replacing bone marrow with firbrotic tissue.
Treatment consists of exogenous EPO or darbepoetin plus iron supplements

132
Q

EPO can cause what?

A

Hypertension

133
Q

Why is blood transfusion not the first line treatment with anemia in CKD?

A

Because it increases the risk of HLA sensitization and future rejection of a transplanted kidney

134
Q

Cardiovascular effects of CKD?

A

HTN is the result of RAAS activation - sodium retention and fluid overload.
Salt and water retention contributes to CHF and pulmonary edema.
CAD is the most common cause of death, assume all CKDs have CAD.
Pericarditis is common with uremia, there is a risk of pericardial effusion and cardiac tamponade.

135
Q

How does CKD affect acid-base balance?

A

Decreased excretion of non-volatile acid contributes to a gap metabolic acidosis. (Remember a gap acidosis is the result of an accumulation of nonvolatile acids, while a non-gap acidosis is the result of loss of HCO3 ions).
The patient will develop a compensatory respiratory alkalosis (hyperventilation).
Acidosis shifts the oxyhemoglobin dissociation curve to the right, this partially compensates for anemia.

136
Q

How does CKD affect serum K+ concentration? Treatment?

A

Hyperkalemia is the result of impaired potassium excretion.
Dialysis is indicated when serum K+ exceeds 6 mEq/L.
Other treatments that reduce K+:
-Glucose (25-50g) + insulin (10-20 units)
-Hyperventilation (for every 10 mmHg decrease in PaCO2, K+ is reduced by 0.5 mEq/L).
-Sodium bicarb (50-100 mEq).

137
Q

How does Calcium chloride help with elevated serum K+ in CKD?

A

Calcium chloride (1g) does not changed serum K+, it raises threshold potential in the myocardium and reduces the risk of lethal dysrhythmias.

138
Q

What are the 2 causes of renal osteodystrophy?

A

Decreased vitamin D production

Secondary hyperparathyroidism

139
Q

Pathophysiology of renal osteodystrophy:

A

An inadequate supply of vitamin D impairs calcium absorption in the GI.
The body responds to hypocalcemia by increasing parathyroid hormone release to demineralization bone to restore Ca.
Additionally, hyperphosphatemia contributes to low serum Ca, phosphate clearance parallels GFR.
The net result is a decreased bone density and increased risk of bone fractures.

140
Q

Respiratory affects of CKD

A

Increased intravascular volume and uremia create a restrictive ventilatory defect.
Volume overload may lead to pulmonary edema.
Metabolic acidosis is compensated by respiratory alkalosis (hyperventilation).

141
Q

Neurologic affects of CKD

A

Uremia impairs nerve conduction.
Autonomic dysfunction contributes to reduced baroreceptor responsiveness (hemodynamic instability) as well as delayed gastric emptying.
Peripheral neuropathies are both sensory and motor, they contribute to silent ischemia.
Central symptoms may be mild (impaired abstract thinking, insomnia) and may progress to severe (seizures, encephalopathy, coma).

142
Q

How does CKD affect infection risk?

A

Impaired white cell function and a low protein diet contribute to the high risk of infection.
Frequent exposure to blood products increases the risk of viral transmission.

143
Q

List 5 indications for dialysis:

A 
Volume overload
Hyperkalemia
Severe metabolic acidosis
Symptomatic uremia
Overdose with a drug that is cleared by dialysis
144
Q

What is the most common complication of dialysis?

A

Hypotension is the most common event during dialysis. This is due to intravascular volume depletion and osmotic shifts.

145
Q

What is the leading cause of death in dialysis patients?

A

Infection

146
Q

Altered responses to anesthetic drugs with impaired renal function are usually due to (5)

A

Active metabolites
Acidosis increases the nonionized fraction
Decreased protein binding increases the free fraction
Impaired elimination of active metabolites
Uremia-induced disruption in the BBB

147
Q

Patients with impaired renal function may experience exaggerated hemodynamic effects due to (3)

A

Antihypertensive medications, specifically ACE inhibitors and ARBs.
Attenuation of SNS tone.
PPV.

148
Q

Do the modern halogenated agents directly cause kidney dysfunction?

A

Although their metabolism liberates free fluoride ions, they do no directly cause renal dysfunction. They can induce hypotension and depress CO, they can indirectly cause renal injury by reducing perfusion.

149
Q

What are the fresh gas flow recommendation for sevoflurane? Why is this?

A

Compound A is produced with sevoflurane is degraded by soda lime. In theory, this can be toxic to the kidneys (no good data). FDA recommends sevoflurane be administered at a rate of 1 L/min for no more than 2 MAC hours. After 2 MAC hours have elapsed, the FGF should be increased to 2 L/min.

150
Q

What factors increase compound A production with sevoflurane?

A

High concentrations over a long period of time
Low FGF
High temperature of CO2 absorbent
Increased CO2 production

151
Q

Opening of the nAChR at the neuromuscular junction from Succinylcholine use can increase serum K+ by how much? For how long? What about with upregulation of extrajunctional receptors?

A

0.5 - 1.0 mEq/L
Up to 10 - 15 minutes
With upregulation of extrajunctional receptors K+ may increase even further.

152
Q

Is Succinylcholine ok to use in patients with renal failure?

A

Renal failure does not cause upregulation in extrajunctional receptors, so SUX is safe in patients with renal failure who have a normal K+ level.

153
Q

Why should SUX not be used as a continuous infusion?

A

The primary metabolite, succinylmonocholine is excreted by the kidney, it is weakly pharmacologically active however it may prolong the period of paralysis.

154
Q

Which class of NMB provides the most predictable duration of action in patients with CKD?

A

Benzylisoquinolines- due to their organ independent elimination, cisatracurium and atracurium are more suitable agents in CKD.

155
Q

Which Benzylisoquinoline produces more laudanosine (CNS stimulant)?

A

Atracurium produces more laudanosine than cisatracurium.

Atracurium also releases Histamine.

156
Q

Discuss the use of aminosteroid neuromuscular blocker in patients with CKD

A

Rocuronium: primarily undergoes hepatobiliary elimination, however it is associated with an unpredictable increased duration of action. Possible causes include a reduced clearance, altered protein binding, and/or an increased potency.
Vecuronium: is metabolized to 3-OH vecuronium. It’s duration is prolonged as a function of decreased clearance and an increased elimination half-life.
Pancuronium: primarily eliminated by the kidneys and has no use in this population.

157
Q

How do you dose NMB-reversal agent for the patient with CKD?

A

Both anticholinesterases and anticholinergics used to reverse NMB undergo renal elimination, and thus share a similar increase in duration. They do not require dosage adjustments.

158
Q

Discuss propofol use with CKD

A

Propofol may need an upward dosage adjustment due to a hyperdynamic circulation and/or disruption of the BBB secondary to uremia.

159
Q

Discuss opioid use with CKD

A

Morphine: metabolized to morphine-6-glucuronide. This product is more potent than morphine, and it relies on renal excretion. Accumulation can contribute to respiratory depression.
Meperidine: metabolized to normeperidine. Accumulation can cause convulsions.
Hydromorphone: metabolized to Hydromorphone-3-glucuronide. This can cause prolonged respiratory depression and myoclonus. Books are inconsistent about this, some say no active metabolite.
Fentanyl, sufentanil, alfentanil, and Remifentanil do not produce active metabolites and are better choices with renal failure.

160
Q

Discuss use of dexmedetomidine with CKD

A

It is biotransformed by the liver and may be used safely in this population. Its duration may be prolonged.

161
Q

What are the 2 mechanisms by which radiographic contrast media cause nephrotoxicity? When do signs of AKI begin? Peak?

A
  1. Ischemic injury due to vasoconstriction in the renal medulla
  2. Direct cytotoxic effects

Signs of AKI begin at 24 - 36 hours and peak between 3 - 5 days.

162
Q

What steps can be taken to prevent nephrotoxicity from radiographic contrast media?

A

Use nonionic iso- or low-osmolality contrast instead of hyperosmolar contrast.
Use the lowest volume of contrast as the procedure will allow.
Withholding other drugs with known nephrotoxic effects.
IV hydration with 0.9% NaCl prior to administration of contrast dye.
Sodium bicarbonate injection or infusion.
N-acetylcysteine is a free radical scavenger, it has fallen out of favor for lack of efficacy.

163
Q

How does Rhabdomyolosis affect renal function?

A

Rhabdomyolosis and myoglobinemia are sequelae of direct muscle trauma, muscle ischemia, or prolonged immobilization.

  • myoglobin binds oxygen inside the myocyte
  • when it is released into the circulation, it is freely filtered at the glomerulus, in the presence of acidic urine (pH <5.6) myoglobin precipitates in the proximal tubule
  • This results in tubular obstruction and acute tubular necrosis
  • In addition, myoglobin scavenges nitric oxide, leading to renal vasoconstriction and ischemia.
164
Q

What substance besides myoglobin is released during muscle injury? What level is associated with increased risk of kidney injury?

A

Creatine phosphokinase

A level in excess of 10,000 units/L

165
Q

How can you prevent or minimize renal injury in the patient with Rhabdomyolosis?

A

Maintenance of renal blood flow and tubular flow with IV hydration
Osmotic diuresis with mannitol
UOP should be kept > 100 - 150 mL/hr
Sodium bicarb and/or acetazolamide to alkalize the urine

166
Q

Which antibiotics are nephrotoxic?

A 
Aminoglycosides (gentamycin, tobramycin, amikacin)
Amphotericin B
Vancomycin
Sulfonamide
Tetracyclines
Cephalosporins
167
Q

What are calcineurin inhibitors, and how do they affect renal function?

A 
Calcineurin inhibitors (cyclosporine and tacrolimus) are immunosuppressant agents used to prevent rejection of transplanted organs. Side effects include hypertension and renal vasoconstriction. 
Sirolimus is a non-calcineurin inhibitor that carries a much lower risk of nephrotoxicity.
168
Q

Transurethral resection of the prostate (TURP) preferred anesthetic?

A

Neuraxial anesthesia - spinal - is the most common approach to TURP, and a T10 level is required.

169
Q

How is irrigation solution absorbed during TURP? Rate? Recommended height of irrigation? Recommended resection time?

A

Through the open venous sinuses of the prostate
10 - 30 mL/min of resection time
No more than 60 cm above OR table
1 hour

170
Q

What is the risk of distilled water when used for irrigation during TURP?

A

Distilled water has an osmolality of zero. This creates a dilutional effect that increases the risk of hyponatremia, hypoosmolality, hemolysis, and hemoglobinuria (renal failure)

171
Q

What is the risk of glycine when used for irrigation during TURP?

A

Glycine metabolism can increase ammonia production, and this can reduce LOC and contribute to encephalopathy.
Glycine is an inhibitory neurotransmitter in the retina, it can cause blindness or blurry vision for up to 24-48 hours.

172
Q

Can 0.9% NaCl and/or LR be used as an irrigation solution during TURP? Why or why not?

A

They are highly ionized so they are good conductors of electricity. Therefore they are contraindicated with unipolar cautery is used.
The introduction of bipolar cautery in newer resectoscopes permits use of ionic solutions.

173
Q

What is TURP syndrome? Classic triad?

A

Absorption of a large volume of hypo-osmolar irrigation solution ->
Hypertension (with increased pulse pressure)
Bradycardia (reflex)
Change in mental status

174
Q

Serum sodium levels and TURP syndrome

A

Na+ < 120 mEq/L increases the risk of complications

Na+ < 110 mEq/L is associated with seizure, coma, and lethal ventricular dysrhythmias

175
Q

Describe the presentation of TURP syndrome

A

CV: HTN, reflex bradycardia, CHF, pulmonary edema, dysrhythmias, MI
CNS: restlessness, N/V, cerebral edema, seizures, coma
Metabolic: hyponatremia
Misc: hemolysis, hypo-osmolality

176
Q

What is the treatment for TURP syndrome?

A

Support oxygenation and CV support
Tell surgeon to abort procedure
Lab data: electrolytes, hematocrit, creatinine, GLU, 12-lead EKG
If Na+ > 120 mEq/L restrict fluids and give loop diuretic furosemide
If Na+ < 120 mEq/L give 3% NaCl at <100 mL/hr - d/c when Na+ > 120
Midazolam may be used for seizures
Intubate and ventilate if difficulty with oxygenation and/or pulmonary edema

177
Q

What happens in serum Na+ is corrected too quickly?

A

Increases risk of central pontine myelinolysis

178
Q

Name 3 other complications of TURP besides TURP syndrome

A

Bladder perforation
Bleeding
Hypothermia

179
Q

Discuss bladder perforation that can occur during TURP

A

Inadvertent stimulation of obturator nerve can cause LE movement which may cause the resectoscope to puncture the bladder wall.
More easily recognized in a conscious patient.
Presentation includes ABD and/or shoulder pain.
A reduction in irrigation fluid return is an early sign of bladder rupture.
TX: supportive - IVF, pressors etc with serial assessment of H&H and transfusion.
Will require emergent suprapubic cystostomy or possible ex lap.

180
Q

Accurate estimation of blood loss during TURP is difficult due to it mixing with irrigation, what is a rough estimate?

A

2-5 mL per minute of resection time

181
Q

Describe how extracorporeal shock wave lithotripsy breaks up kidney stones

A

The acoustic impedance of water and human tissue is roughly similar, the shock wave moves through the body until it reaches the body-stone interface

182
Q

List the absolute and relative contraindications to ECSW lithotripsy

A

Absolute: pregnancy, risk of bleeding (disorder or anticoagulation)
Relative: pacemaker/ICD, calcified aneurysm of the aorta or renal artery, untreated UTI, obstruction below the stone, morbid obesity

183
Q

How does ECSWL affect cardiac conduction? What is done to minimize this risk?

A

The shock wave can produce dysrhythmias and the pulse wave is timed to the R wave on EKG to minimize R-on-T phenomena

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