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APEX-KLE > KLE-Kidney > Flashcards

KLE-Kidney Flashcards

1
Q

What are the 2 divisions of the kidney

A

Cortex (outer)

Medulla (inner pyramids)

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2
Q

Which parts of the nephron are in the renal cortex

A

Glomeruli
Bowman’s capsule
Proximal tubules
Distal Tubules

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3
Q

Which parts of the nephron are in the renal medulla

A

Loops of Henle

Collecting ducts

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4
Q

What are the 6 major functions of the kidney

A
  1. Maintenance of extracellular volume and composition
  2. BP regulation
  3. Excretion of toxins and metabolites
  4. Maintenance of A-B balance
  5. Hormone production
  6. Blood glucose homeostasis
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5
Q

3 mechanisms by which the kidney maintains extracellular volume and composition

A
  1. Aldosterone controls volume by Na+ and H2O reabsorption
  2. ADH controls plasma osmolarity by H2O reabsorption ONLY
  3. Regulation of K, Cl, PO3, Mg, H, HCO3, glucose, and urea
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6
Q

How do the kidneys manage long-term BP control

A

This is carried out by the thirst mechanism (intake) and na+ and H2O excretion (output)

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7
Q

How do the kidneys manage intermediate-term BP control

A

This is carried out by the renin-angiotensin-aldosterone system

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8
Q

Where are renin, angiotensinogen, and aldosterone produced

A 
Renin = juxtaglomerular cells
Angiotensinogen = liver
Aldosterone = adrenal cortex
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9
Q

How do the kidneys manage short-term control of the BP

A

Bia the baroreceptor reflex

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10
Q

What type of biotransformation can take place in the kidneys

A

Phase 1 and 2

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11
Q

How do the kidneys excrete toxins and metabolites

A

Via glomerular filtration and tubular secretion

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12
Q

What is the kidneys role in maintenance of A-B balance

A

Excretion of non-volatile acids

Excretion of H+ in tubular fluid when needed

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13
Q

What hormones do the kidneys produce

A
  1. Erythropoietin
  2. Prostaglandins
  3. Calcitriol
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14
Q

What stimulates erythropoietin release and from where

A

Stimulation = inadequate O2 delivery i.e. anemia, hypovolemia, hypoxia

Release = from kidneys

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15
Q

What is the function of erythropoietin

A

To stimulate stem cells in the bone marrow to produce erythrocytes

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16
Q

How does severe kidney disease affect erythrocytes

A

It reduces EPO production leading to chronic anemia

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17
Q

What prostaglandins are produced by the kidneys and their function

A

PGE2/PGI2 = vasodilation of renal arteries

Thromboxane A2 = vasoconstrict renal arteries

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18
Q

What is the action of the kidneys on Ca++ levels

A

Kidneys synthesize converted calciferol (inactive Vit D3) to calcitriol (active Vid D3) with PTH regulation which then helps increase Ca++ by 3 mechanisms

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19
Q

What are the 3 mechanisms that calcitriol can affect serum Ca++ levels

A
  1. Stimulate Ca++ absorption from intestines (increase level)
  2. Prevent Ca++ excretion from kidneys (increase level)
  3. Increases Ca++ deposition in bones
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20
Q

What impact does PTH have on the kidneys

A

It regulates the process of converting 25-hydroxycholecalciferol to 1,25-dihydroxycholecalciferol (calcitriol- Vit D3a)

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21
Q

How do the kidneys contribute to glucose homeostasis

A

They can synthesize glucose from amino acids (gluconeogenesis)

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22
Q

What hormone controls plasma osmolarity

A

ADH - by reabsorbing water but NOT Na+

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23
Q

What hormone controls extracellular fluid volume

A

Aldosterone - by reabsorbing Na+ AND H2O

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24
Q

What percentage and volume of cardiac output do kidneys receive

A

20-25%

1,000-1,250 mL/min

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25
Q

What percentage of the blood delivered to the kidneys is processed by the glomerulus vs circulated via peritubular capillaries

A

20% via glomerulus

80% via peritubular capillaries

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26
Q

What percent of the ultrafiltrate, originally from glomerular filtration, is reabsorbed

A

99%

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27
Q

What is the distribution of blood flow to the following portions of the kidney:
Cortex
Medulla/juxtamedullary nephron

A

Cortex = 90%

Medulla/juxtamedullary nephron = 10%

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28
Q

What is the PaO2 in the following portions of the kidneys:
Cortex
Medulla/juxtamedullary nephron

A

Cortex = 50 mmHg

Medulla/juxtamedullary nephron = 10 mmHg

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29
Q

Why is the renal medulla more sensitive to ischemia

A

Because the PaO2 is ~10 mmHg

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30
Q

How does renal blood flow change during the life-span

A

It decreases 10% per decade of life after 50-years

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31
Q

Equation for renal blood flow

A

RBF = (MAP - renal venous pressure) / renal vascular resistance

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32
Q

Describe the arterial renal blood flow starting at the renal artery

A

renal a. => interlobar a. => arcuate a. => interlobular a. => afferent aa => glomerular capillary bed => efferent aa => peritubular capillary beds

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33
Q

Describe the venous renal blood flow starting at the peritubular capillary bed

A

Peritubular cap bed => venules => interlobular v => arcuate v => interlobar v => renal segmental v => renal vein

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34
Q

What is glomerular filtration dependent on when MAP is outside of the range of autoregulation

A

Glomerular filtration becomes pressure dependent

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35
Q

How does autoregulation of the kidneys affect renal perfusion

A

Low perfusion = autoreg increases RBF by decreasing renal vascular resistance

High perfusion = decrease RBF by increasing renal vascular resistance

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36
Q

What are 6 processes that aid in renal autoregulation

A
  1. Myogenic mechanism*
  2. Juxtaglomerular apparatus and tubuloglomerular feedback*
  3. RAAS
  4. Prostaglandins
  5. Atrial natriuretic peptide
  6. SNS
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37
Q

Describe the impact of myogenic mechanisms on renal autoregulation

A
  1. If renal a. pressure is high, myogenic mech constricts the afferent aa. to protect glomerulus from excessive pressure
  2. When renal a. pressure is low, myogenic mech dilates afferent aa. to increase BF
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38
Q

Where is the juxtaglomerular apparatus located

A

Distal tubule in the region that passes between the afferent and efferent aa.

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39
Q

What is the mechanism by which the tubuloglomerular feedback system autoregulates renal blood flow

A

It gains feedback about Na+ and Cl- composition in the distal tubule affecting arteriolar tone
This creates a negative feedback loop to maintain RBF

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40
Q

Where do the kidneys receive SNS innervation

A

T8-L1

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41
Q

How does the SNS impact RBF during the perioperative period

What is the kidney at increased risk for

A

Surgical stress and catecholamine admin cause the SNS to reduce RBF. This causes vasoconstriction and Na+ retention
The effects of this altered physiology can last for days postop, leading to oliguria and edema

Increased risk:
Ischemic injury and effects of nephrotoxic drugs

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42
Q

What renal structures are innervated by the SNS

A

Afferent and efferent aa

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43
Q

What change alerts the juxtaglomerular apparatus to decreased RBF
What is the response

A

Decreased GFR reduces Na+ and Cl- delivery

The afferent aa is then dilated to restore GFR

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44
Q

What structure senses alterations in Na+ and Cl- concentrations in the juxtaglomerular apparatus

A

The macula densa

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45
Q

When low Cl- concentration is detected by the macula densa, what is the response

A

Renin release from the JG cells, this activates the RAAS

Ang 2 constricts the efferent aa, increasing GFR

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46
Q

What 2 JGA mechanisms increase GFR

A

Dilation of afferent aa when Na/Cl delivery is reduced

Constriction of efferent aa when Cl- concentration is low

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47
Q

What is the relationship of urine output and MAP

A

The relationship is linear
UO typically halts when MAP<50 mmHg
UO is NOT auto-regulated

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48
Q

What are 3 conditions that stimulate renin release

A
  1. Beta-1 stimulation (SNS activation)
  2. Hypovolemia (decreased renal perfusion)
  3. Hyponatremia (tubuloglomerular feedback)
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49
Q

Describe the RAAS

A

Angiotensinogen is produced and released by the liver
Renin hydrolyzes angiotensinogen into Angiotensin I
Angiotensin I is converted to A-II in the lungs with ACE

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50
Q

How does angiotensin II affect BP

A
  1. Vasocontraction via increased venous and arterial tone
  2. Increased aldosterone via synthesis in adrenal cortex zona glomerulosa
  3. SNS activation via catecholamine output from adrenal medulla
  4. Increase ADH output from posterior pituitary
  5. Increase thirst
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51
Q

What are causes of decreased renal perfusion pressure that can increase renin release

A
  1. Hemorrhage
  2. PEEP
  3. CHF
  4. Liver failure w/ ascites
  5. Sepsis
  6. Diuresis
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52
Q

Where is aldosterone produced

A

Zona glomerulosa of the adrenal gland

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53
Q

What 2 action does aldosterone have in the kidneys

A
  1. Stimulates Na/K-ATPase in principal cells of distal tubules and collecting ducts
  2. Facilitates Na+ and H2O reabsorption and K+/H+ excretion
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54
Q

What 2 electrolyte imbalances can stimulate aldosterone release

A
  1. Hyperkalemia

2. Hyponatremia

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55
Q

What is Conn’s disease

A

Disease of excess aldosterone production

Causes Na+ retention and K+ loss

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56
Q

Stimulation of which adrenergic receptor increases renin release

A

Beta-1

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57
Q

Where is ADH produced

A

Hypothalamus (supraoptic and paraventricular nuclei)

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58
Q

Where is ADH released

A

Posterior pituitary gland

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59
Q

What are 2 other names for ADH

A

Vasopressin

Arginine vasopressin

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60
Q

What are the 2 mechanisms that control ADH release

A
  1. Increased osmolarity of ECF

2. Decreased blood volume

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61
Q

How does an increased osmolarity trigger ADH release

A
  1. Increased Na+ concentration shrinks osmoreceptors in hypothalamus
  2. ADH is transported from hypothalamus to posterior pituitary
  3. ADH is released systemically
  4. Thirst reflex is activated (to increase serum osmo)
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62
Q

How does decreased blood volume trigger ADH release

A

Hypovolemia unloads the baroreceptors in the carotid sinuses, transverse aortic arch, great veins, and RA.
This stimulates ADH release via afferent messages from CN9 and CN10

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63
Q

How does ADH restore blood volume

A
  1. Stimulates V1 receptor causing vasoconstriction of peripheral vasculature and increasing IP3
  2. Stimulates V2 receptor in collecting ducts, increasing cAMP
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64
Q

How does ADH cause vasoconstriction

A

Stimulates V1 receptors in periphery. This increases IP3, DAG, and Ca++ leading to vasoconstriction

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65
Q

What anesthetic effects can increase ADH release

A
  1. PEEP
  2. PPV
  3. HoTN
  4. Hemorrhage
    (anything that affects arterial BP or venous blood return decreasing CO)
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66
Q

How does ADH facilitate water reabsorption and affect osmolarity

A

It upregulates aquaporin-2 channels in the collecting ducts (medulla)

This increased water reabsorption (w/o Na+), reducing plasma osmolarity and increasing urine osmolarity

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67
Q

What is the physiologic response of the V1 and V2 receptors

A 
V1 = peripheral vasoconstriction
V2 = expansion of plasma volume via H2O reabsorption in kidneys
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68
Q

What are 3 mechanisms that promote renal vasodilation

A
  1. Prostaglandins
  2. Natriuretic peptide
  3. Dopamine receptors
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69
Q

What is the role of prostaglandins in the kidneys

A

Promoting renal blood flow following production in the afferent aa.

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70
Q

Why do NSAIDs impact renal blood flow

A

They block cyclooxygenase which ultimately inhibits renal prostaglandin vasodilatory effects

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71
Q

What mediators are produced by the myocardium in response to atrial distension

A

Atrial and brain natriuretic peptide

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72
Q

What is the role of natriuretic peptides

A
  1. Inhibit renin release (negative feedback on RAAS)

2. Promote Na+ and H2O excretion into collecting ducts

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73
Q

What dopamine receptors are present in the kidneys

A

DA1

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74
Q

What is the location and 2nd messenger of DA1 receptors

A

Location = renal vasculature, tubules

2nd messenger = Increased cAMP

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75
Q

What is the role of DA1 receptors in the kidney

A
  1. Vasodilation
  2. Increased RBF
  3. Increased GFR
  4. Diuresis
  5. Na+ excretion
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76
Q

What is the MOA and class of fenoldopam

A 
Class = DA1 receptor agonist
MOA = increases renal blood flow via renal vasodilation, increased GFR, and Na+ excretion
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77
Q

What are the portions of the nephron starting at the glomerulus

A

Glomerulus => Bowman’s capsule => proximal convoluted tubule => loop of Henle (descending loop ==> ascending loop thin/thick) => Distal convoluted tubule => collecting duct

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78
Q

What is the normal
GFR
Glomerular filtration fraction

A

GFR = 125 mL/min

Filtration fraction = 20%

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79
Q

What substances are freely filtered at the glomerulus.

What substances are not

A

Filtered = Water, electrolytes and glucose

Not filtered = plasma proteins (albumin)

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80
Q

How does the glomerular filtrate differ from plasma

A

It does not contain plasma proteins, erythrocytes, or WBCs

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81
Q

What does kidney disease destroy

A

The basement membrane allowing proteins to enter the tubules

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82
Q

How is the net filtration pressure of the nephron determined

A

NFP = glomerular hydrostatic P - Bowman’s capsule hydrostatic P - Glomerular oncotic P

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83
Q

What factor is the most important determinant of GFR

A

Glomerular hydrostatic pressure

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84
Q

What are the 3 factors that determine glomerular hydrostatic pressure

A
  1. Arterial BP
  2. Afferent arteriole resistance
  3. Efferent arteriole resistance
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85
Q

How does arterial BP affect GFR

A

increased MAP = increased GFR

Decreased MAP = decreased GFR

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86
Q

How is the kidney protected from hypo-hyperperfusion

A

Autoregulation, as long as the BP are within the upper and lower limits

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87
Q

How does afferent aa resistance affect GFR

A 
Constriction = decreased GFR
Dilation = increased GFR
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88
Q

How does efferent aa resistance affect GFR

A

Constriction:

  • mild = decreased peritubular flow, increased GFR
  • Excessive = reduced RBF and GFR

Dilation = increases peritubular flow and decreases GFR

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89
Q

Define the following in terms of renal physiology
Reabsorption
Secretion
Excretion

A

Reabsorption = from tubule (pee) to peritubular capillaries (circ)

Secretion = form peritubular capillaries (circ) to tubules (pee)

Excretion = removed from body in urine

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90
Q

What is the equation of urine production

A

Urinary excretion rate = filtration - reabsorption + secretion

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91
Q

What is the primary function of the PCT

A

Bulk reabsorption of solutes and water

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92
Q

Where does the most Na+ get reabsorbed in the nephron

A

The PCT (65%)

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93
Q

What ions are reabsorbed in bulk at the PCT and how

A

Active transport:
Na+

Na+ Co-transport:
K+
Cl-
HCO3

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94
Q

What substances are secreted into the PCT via Na+ counter-transport

A

Organic bases
Acids
H+

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95
Q

What organic acids and bases are exchanged for Na+ counter-transport in the PCT

A 
Bile salts
Uric acid
Catecholamines
Toxins
Some drugs
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96
Q

What is the primary function of the descending loop of Henle

A

Forming concentrate or dilute urine via separation of Na+ and H2O handling

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97
Q

What is the function of the vasa recta

A

To maintain the medullary osmotic gradient

Vasa recta is the vasculature surrounding the loop of Henle

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98
Q

What are the 2 countercurrent systems that maintain the hyperosmotic peritubular insterstium

A

Loop of Henle = creates the gradient

Vasa recta = maintains the medullary osmotic gradient

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99
Q

Describe the permeability of the descending limb of the loop of Henle

A

Highly permeable to water (20% of H2O reabsorption occurs here)
Modestly permeable to ions

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100
Q

What happens to osmolarity along the descending loop of Henle

A

It increases from 300 to 1500 at the renal pelvis

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101
Q

Describe the permeability of the ascending loop of Henle

A

The thin and thick segments are NOT permeable to water

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102
Q

What is the most important ion pump in the ascending loop of Henle

A

The Na-K-Cl cotransporter

Pumps ions from tubular fluid into peritubular interstitum

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103
Q

What section of the nephron is the target of loop diuretics

A

The ascending loop, Na-K-Cl cotransporter

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104
Q

Where is the second greatest site of Na+ reabsorption

A

The ascending loop (via Na-K-Cl cotransporter)

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105
Q

What ion is excreted in the ascending tubule via what mechanism

A

H+ via the Na-H exchange mechanism

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106
Q

What actions occur in the distal convoluted tubule

A

Fine tuning of solute concentration

-5% of Na+ is reabsorbed (along with K, Cl, HCO3 via co-transport)

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107
Q

Which sections of the nephron are impermeable to H2O

A
  1. Ascending loop

2. Late distal tubule (except w/ aldosterone or ADH)

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108
Q

Which portion of the nephron do aldosterone and ADH act

A

The DCT and collecting duct

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109
Q

What portion of the nephron does PTH influence Ca++ reabsorption

A

DCT

110
Q

What portion of the nephron does atrial natriuretic peptide act

A

Collecting duct

111
Q

What are actions that occur at the collecting duct

A
  1. Reabsorb 5% of Na+
  2. ADH and aldosterone action
  3. ANP inhibits water/Na+ reabsorption
  4. Adjusts H+ concentration
112
Q

Where is the site of action of acetazolamide

MOA

A

The proximal tubule

MOA = Carbonic anhydrase is inhibited, reducing HCO3-, Na+ and H2O reabsorption

113
Q

What are 3 clinical uses of acetazolamide

A
  1. Open-angle glaucoma
  2. High altitude sickness
  3. Central sleep apnea
114
Q

What are complications of acetazolamide use

A
  1. Metabolic acidosis
  2. Hypokalemia
  3. Exacerbated CNS depression in COPD (d/t loss of HCO3
115
Q

What is the site and mechanism of action for osmotic diuretics in the nephron

A

They undergo filtration but not reabsorption

Inhibition of water reabsorption in the PCT and loop of Henle

116
Q

What is the site and mechanism of action of loop diuretics

Examples

A

The ascending limb of the loop of Henle
They act on Na-K-2Cl transporter disrupting the tubules’ ability to reabsorb Na+
Ex: furosemide, bumetanide, ethacrynic acid

117
Q

What ions are lost with loop diuretic use

A

Na, K, Ca, Mg, Cl

118
Q

What is the site and mechanism of action of thiazide diuretics
Examples

A 
Site = Distal tubule
MOA = Inhibition of Na-Cl co-transporter in DCT activating the Na-Ca antiporter. This increases Ca++ reabsorption and serum Ca++

Examples: hydrochlorothiazide, chlorthalidone, metolazone

119
Q

What is a unique side effect of thiazide diuretics

A

They can cause hyperglycemia

120
Q

What type of a acid-base disturbance can result from thiazide and loop diuretics

A

Hypokalemic, hypochloremic metabolic alkalosis

121
Q

Metabolic acidosis can be the result of what kind of diuretic use

A

Carbonic anhydrase inhibitor (acetazolamide)

Potassium-Sparing diuretics

122
Q

What is the site and mechanism of action of potassium-sparing diuretics
Examples

A

Site = Collecting ducts

MOA = inhibition of K+ secretion and Na+ reabsorption

123
Q

How does spironolactone differ from other potassium-sparing diuretics

A

It is an aldosterone antagonists

Blocking aldosterone at mineralocorticoid receptors, inhibiting K secretion and Na+ reabsorption

124
Q

What are 2 reasons amiloride is administered

A
  1. To reduce K+ loss in a patient receiving a loop or thiazide diuretics
  2. Secondary hyperaldosteronism
125
Q

5 Side effects of potassium-sparing diuretics

A
  1. Hyperkalemia
  2. Metabolic acidosis
  3. Gynecomastia
  4. Libido changes
  5. Nephrolithiasis
126
Q

What are 3 drug classes that increase the risk of hyperkalemia in a patient on potassium-sparing diuretics

A
  1. NSAIDs
  2. Beta-blockers
  3. ACE inhibitors
127
Q

What 2 functions are assessed with renal function tests

A
  1. Glomerular function

2. Tubular function (concentrating ability)

128
Q

Which tests assess glomerular function

A

Blood urea nitrogen
Serum Creatinine
Creatinine clearance

129
Q

Which tests assess tubular function (concentrating ability)

A 
TESTS ON URINE
Fractional excretion of Na+
Urine osmolality
Urine Na+ concentration
Urine specific gravity
130
Q

What does a low BUN indicate

A
  1. Overhydration

2. Decreased urea production (malnutrition or liver dz)

131
Q

What does can an elevated BUN indicate

A
  1. Dehydration
  2. Increased protein input (GIB, hematoma breakdown)
  3. Catabolism (Trauma, sepsis)
  4. Decreased GFR
132
Q

What is creatinine

A

A metabolic byproduct of creatin breakdown which is produced by skeletal muscle

133
Q

Why is BUN a better indicator of uremic symptoms than a measure of GFR

A

B/c it underdoes filtration and reabsorption

134
Q

Why is creatinine a better indicator of GFR

A

It undergoes filtration only (no reabsorption)

135
Q

What does a 100% increase in creatinine indicate for the GFR

A

a 50% reduction

136
Q

What is the significance of BUN:crt ratio

A

Helps evaluate the state of hydration

137
Q

What do the following BUN:creatinine values indicate
10:1 =
>20:1 =

A 
10:1 = normal ratio
>20:1 = prerenal azotemia (increased nitrogen compounds)
138
Q

What is the most useful indicator of GFR

A

Creatinine clearance

139
Q

What do the following values of Fractional excretion of Na+ indicate
Fe(Na+) <1%
Fe(Na+) >3%

A

Fe(Na+) <1% = Prerenal azotemia; more Na+ conserved relative to Crt cleared
Fe(Na+) >3% = Impaired tubular function; more Na+ excreted to amount of Crt cleared

140
Q

What is the significance of fractional excretion of Na

A

It relates Na+ clearance to creatinine clearance

141
Q

What does an elevated urine sodium indicate

A

Failing kidneys

Kidney failure wastes Na+

142
Q

What is the most common cause of perioperative kidney injury

A

ischemia-reperfusion injury

143
Q

What patient characteristics increase the risk of perioperative AKI

A
  1. Pre-existing kidney dz
  2. Prolonged renal hypoperfusion
  3. CHF
  4. Advanced age
  5. Sepsis
  6. Jaundice
  7. High risk surgery (aortic clamp)
144
Q

What is the common cause of oliguria in the perioperative period

A

prerenal origin

145
Q

Why is urine output not a reliable surrogate for perioperative renal perfusion

A

Because perioperative stress increases ADH release which causes H2O and Na+ reabsorption

146
Q

What are the classes of renal injury considered with the RIFLE criteria

A 
Risk
Injury
Failure
Loss
End-Stage
147
Q

What are the criteria for renal injury RIFLE classes

A

Risk = increase Cr >1.5x base; UOP<0.5 mL/kg/hr >6 hrs

Injury = increase Cr >2x base; UOP <0.5 ml/kg/hr >12 hrs

Failure = increase Cr>3x base or Cr>4 mg/dL; UOP <0.3 ml/kg/hr >12 hrs, Anuria >12hr

Loss = need for RRT >4 wks

End-stage = need for RRT>3 mo

148
Q

What are the stages of the AKIN classification of renal injury

A

Risk = Cr increase >1.5-2x base; UO<0.5 ml/kg/hr >6 hrs

Injury = Increase Cr>2-3x base; UOP <0.5 ml/kg/hr >12 hrs

Failure = Increase Cr >3x base, or RRT needed; UOP<0.3 ml/kg/hr >12 hr or anuria

149
Q

What are 5 causes of prerenal injury

A

Hypoperfusion d/t:

  1. Hypovolemia
  2. Decreased CO
  3. Systemic vasodilation
  4. Renal vasoconstriction
  5. Increased intra-abd pressure
150
Q

What is treatment for prerenal injury

A
  1. Restoration of RBF w/ IVF, PRBCs, and hemodynamic support

2. Renal prostaglandins for vasodilation. Avoid NSAIDs

151
Q

How can treatment for prerenal injury be diagnoses

A

Improvement in UOP following IVF bolus

152
Q

What is the cause of intrinsic kidney injury

A

Parenchymal damage

153
Q

What does 80% of the O2 delivered to the kidney feul

A

Ionic gradients in the nephron

154
Q

What section of the kidney is injured with intrinsic renal damage

A

Medulla d/t medullary ischemia

155
Q

What are intrinsic causes of acute tubular necrosis

A
  1. Ischemia

2. Nephrotoxic drugs

156
Q

What are factors that increase intrinsic renal injury

A
  1. Renal medulla is more susceptible to ischemic insult
  2. Renal tubules require O2 to support ionic transfer between tubular and peritubular fluids
  3. Use of nephrotoxic drugs i.e. IV contrast die, abx, and NSAIDs compounds pre-renal injury
157
Q

What is the treatment for intrinsic kidney injury

A
  1. Restore renal perfusion

2. Supportive

158
Q

What is the cause of postrenal injury

Treatment

A

Obstruction between collecting system and urethra

Treatment = relieve obstruction

159
Q

5 factors that increase prerenal injury

A
  1. Intravascular volume depletion
  2. Decreased CO
  3. Systemic vasodilation
  4. Renal vasoconstriction
  5. Increased abd pressure
160
Q

What are 5 factors that increase intrinsic renal injury

A
  1. Tubular injury
  2. Tubulointerstitial injury
  3. Glomerular injury
  4. Renal vasculature
  5. Large vessels
161
Q

What are 6 factors that contribute to tubular injury

A
  1. Ischemia from hypoperfusion
  2. Myoglobin
  3. Free hgb (transfusion rxn)
  4. Antibiotics
  5. Contrast agents
  6. Chemotherapeutics
162
Q

What are 3 factors that contribute to tubulointerstitial injury

A
  1. Acute allergic interstitial nephritis
  2. Infection
  3. Infiltration
163
Q

What are 3 factors that contribute to glomerular injury

A
  1. Inflammatory dz
  2. Hemolytic uremic syndrome
  3. Thrombotic thrombocytopenic purpura
164
Q

What are 4 factors that contribute to renal vasculature issues and intrinsic renal injury

A
  1. Toxemia of pregnancy
  2. Hypercalcemia
  3. Contrast agents
  4. MH
  5. Scleroderma
165
Q

What are 4 factors that contribute to large vessel issues causing intrinsic kidney injury

A
  1. Thrombosis
  2. Vasculitis
  3. Dissection
  4. Trauma
166
Q

How can prerenal azotemia be reduced

A
  1. Maintain MAP>65 mmHg

2. Hydration

167
Q

What type of fluid can increase risk of renal morbidity

A

Fluids containing hydroxyethyl starches

168
Q

What acid base imbalance is caused by excessive o.9% NaCl

A

Hyperchloremic metabolic acidosis

169
Q

How can diuretic use impact renal health in AKI

A

Attempting to convert oliguric to nonoliguric AKI can increase the risk of additional renal injury

170
Q

How do alpha-1 agonists impact RBF in healthy vs septic pts

A
  1. Healthy pts can have reduced RBF
  2. Septic pts can benefit if MAP is supported
    - Renal perfusion outweigh renal vasoconstrictive effects
171
Q

How does vasopressin use affect RBF

A
  1. Preferentially constricts efferent arteriole

2. Maintains GFR and UOP

172
Q

How does dopamine affect renal perfusion

A

Renal dose of dopamine does not prevent or treat AKI

173
Q

What nephrotoxic drugs should be avoided in pts at risk for AKI

A
  1. Aminoglycoside abx
  2. Amphotericin B
  3. NSAIDs
  4. Diuretics unless pt is fluid overloaded
174
Q 
What is the type and GFR associated with the following stages of kidney disease
1
2
3
4
5
A 
1 = normal, GFR >90 mL/min
2 = mild decrease; GFR 60-80 ml/min
3 = moderate decrease; GFR 30-59 ml/min
4 = severe decrease; GFR 15-29 ml/min
5 = failure; <15 ml/min (req dialysis)
175
Q

What are s/sx of uremic syndrome

A
  1. Anemia
  2. Fatigue
  3. N/V
  4. Anorexia
  5. Coagulopathy
176
Q

How is BUN level associated with uremic symptoms

A

It parallels symptoms and can guide management

177
Q

How is bleeding affected by uremia

A
  1. Increase risk of bleeding

2. Bleeding time is increased

178
Q

How are coagulation tests affected by uremia

A

PT, PTT, and plt counts are normal

Bleeding time is increased

179
Q

How is increased bleeding time treated with uremia

A

Desmopressin is first-line treatment

180
Q

What treatment can improve bleeding time in uremic pts

A
  1. Desmopressin

2. Dialysis

181
Q

What type of anemia do CKD pts have

A

Normochromic normocytic anemia from decreased erythropoietin production

182
Q

What is the treatment for CKD associated anemia

A

Exogenous EPO or darbepoetin iron supplementation

183
Q

Why is blood transfusion not a first-line treatment for CKD related anemia

A

It increases the risk of HLA sensitization increasing the risk for future rejection of transplanted kidney

184
Q

What is the cause of ckd related HTN

A

RAAS activation leading to sodium retention and fluid overload

185
Q

What are CV effects of CKD and their cause

A 
Effects = CHF, pulm edema
Cause = Na+ and H2O retention
186
Q

What is the most common cause of death in CKD pts

A

CAD, assume all CKD pts have CAD

187
Q

What cardiac pathology is common with uremia

A

Pericarditis is common

Risk for pericardial effusion and cardiac tamponade

188
Q

What is the etiology of acid-base imbalance in CKD

A

decreased excretion of non-volatile acid

Contributes to gap metabolic acidosis from accumulation of non-volatile acids

189
Q

How does acidosis in CKD affect the oxyhgb dissociation curve

A

Shift right

Partially compensates for anemia

190
Q

What is the etiology of hyperkalemia in CKD

When is dialysis indicated

A

D/t impaired K excretion

Dialysis when K> 6 mEq//L

191
Q

What are additional treatments for hyperkalemia

A
  1. Glucose (25-50 g)+ insulin (10 - 20 units)
  2. hyperventilate
  3. NaHCO3 50 - 100 mEq
192
Q

How does hyperventilation affect serum K

A

For every 10 mmHg in PaCO2 serum K decreases by 0.5 mEq/L

193
Q

Why is CaCl (1 g) given with elevated serum K

A

It raises the threshold potential reducing the risk of lethal dysrhythmias

194
Q

How does CKD affect skeletal structure

A

Causes osteodystrophy

195
Q

What is the cause of renal osteodystrophy

A
  1. Decreased vitamin D production

2. Secondary hyperparathyroidism

196
Q

What is the pathophysiology of CKD associated Vit D under production and osteodystrophy

A
  1. Inadequate supply of Vit D impairs Ca++ absorption in the GI tract
  2. Increased PTH release which demineralizes bone to restore serum Ca++
  3. Result is decreased bone density
197
Q

How is phosphate level associated with CKD

A

It is elevated which contributes to low serum Ca++

Phosphate clearance is inversely proportion to GFR
low GFR = HI phosphate

198
Q

What respiratory pattern is a result of uremia

A

Increased intravascular volume creates restrictive ventilatory defect

199
Q

Respiratory effects of CKD

A
  1. Restrictive ventilatory defect
  2. Pulmonary edema
  3. Hyperventilation d/t respiratory compensation of met acidosis
200
Q

What is a neurologic effect of uremia

A
  1. Impaired nerve conduction
  2. Peripheral neuropathy
  3. Autonomic dysfunction
201
Q

Result of autonomic dysfunction d/t CKD

A

Contributes to reduce baroreceptor responsiveness

Delays gastric emptying

202
Q

What is the risk of peripheral neuropathy in the CKD pt

A

Since it is both sensory and motor, this contributes to silent MI

203
Q

How does CKD affect risk for infection

A

Impaired WBC function and low protein diets contribute to the high risk of infection

Blood products increase risk of viral transmission

204
Q

What are the 5 indications for dialysis in CKD

A
  1. Volume overload
  2. Hyperkalemia
  3. Sever metabolic acidosis
  4. Symptomatic uremia
  5. OD w/ drugs that are cleared renally
205
Q

What are 5 reasons anesthetic drugs have altered response in CKD

A
  1. Active metabolites
  2. Acidosis
    increases nonionized fraction (decreasing excretion)
  3. Decreased protein binding increases free fraction
  4. Impaired elimination of active metabolites
  5. Uremia-induced disruption of BBB
206
Q

What are 3 exaggerated hemodynamic effects associated with altered anesthetic drug action in CKD

A
  1. Antihypertensive medications especially ACE-i and ARBs
  2. Attenuation of SNS tone
  3. PPV
207
Q

How do halogenated anesthetics contribute to AKI

A

They can reduce renal perfusion (systemic vasodilation) coupled with renal vasoconstriction from vasopressors and injury from nephrotoxic agents

208
Q

Is succinylcholine safe to use in renal failure

A

Yes.
It can be used when serum K+ is normal. Pts don’t have upregulation of extrajunctional ACh receptors to increase K+ greater than normal

209
Q

Why should succinylcholine infusion be avoided in renal disease

A

The primary metabolite (succinylmonocholine) is excreted by the kidneys, so paralysis may be prolonged d/t its weak action

210
Q

Which NMB drugs are most appropriate in renal failure and why

A

Benzylisoquinolines (cisatracurium and atracurium)

Organ independent elimination

211
Q

What are causes of the potential for rocuronium increased duration of action

A
  1. reduced clearance
  2. altered protein binding
  3. increased potency
212
Q

Which aminosteroids are safe for use in renal failure

A

Rocuronium is most appropriate

Vec and Panc should not be used

213
Q

Why should vecuronium and pancuronium be avoided in renal failure

A

Vec = 3-OH vecuronium metabolite increased duration of action d/t decreased clearance and increase elim HL

Panc = primarily eliminated by kidneys

214
Q

What effects does renal disease have on reversal agents

A
  1. anticholinesterases and anticholinergics undergo renal elimination and can have increased duration
  2. Sugammadex is not recommended in pts with severe renal impairment
215
Q

Which opioids should be avoided in renal disease

A
  1. Morphine

2. Meperidine

216
Q

Why should morphine be avoided in renal disease

A

The active metabolite (morphine-6-glucuronide) i smore potent than morphine and relies on renal excretion
Accumulation can cause respiratory depression

217
Q

Why should meperidine be avoided in renal disease

A

It is metabolized into normeperidine

Accumulation of the metabolite can cause convulsions

218
Q

Which opioids are safe to use in renal disease

A
  1. Fentanyl
  2. Sufentanil
  3. alfentanil
  4. remifentanil
  5. hydromorphone (controversial potential metabolite)
219
Q

What are 4 factors that accelerate compound A production with Sevo use

A
  1. High concentration for prolong time
  2. Low FGF
  3. Hi temp of CO2 absorbent
  4. Increased CO2 production
220
Q

How does radiographic contrast media cause nephrotoxicity

A
  1. Ischemic injury d/t vasoconstriction in renal medulla

2. Direct cytotoxic effect

221
Q

What are 6 methods to prevent contrast-induced nephropathy

A
  1. Use nonionic iso- or low-osmolar contrast instead of hyperosmolar contrast
  2. Lowest contrast volume
  3. Withhold other nephrotic drugs
  4. Hydrate w/ 0.9% NaCl p/t contrast
  5. HCO3 administration
  6. N-acetylcysteine
222
Q

How does N-acetylcysteine impact contrast-induced nephropathy

A

It is a free radical scavenger but has been determined to be less efficacious

223
Q

How does increased myoglobin impact the kidneys

A

It can precipitate in the proximal tubules causing tubular obstruction and ATN

224
Q

Why does myoglobin cause ATN

A

It is freely filtered by the glomerulus.

In the presence of acidic urine (pH<5.6), myoglobin precipitates in the proximal tubule causing obstruction and ATN

225
Q

How does myoglobin cause vasoconstriction

A

It scavenges NO leading to renal vasoconstriction and ischemia

226
Q

What wastes are released during rhabdomyolysis that can cause kidney injury

A
  1. Myoglobin

2. Creatine phosphokinase

227
Q

What are AKI preventative strategies during rhabdomyolysis

A
  1. IVF hydration to maintenance of RBF and tubular flow
  2. Osmotic diuresis w/ mannitol
  3. UOP >100-150 mL/hr
    NaHCO3 and acetazolamide to alkalize urine
228
Q

What medications are given to the pt w/ rhabdomyolysis

A
  1. Mannitol
  2. NaHCO3
  3. Acetazolamide
229
Q

How does sevoflurane impair renal function

A
  1. Compound A

2. Free fluoride ions

230
Q

How does sevo metabolism affect renal function

A
  1. 5% of sevo is metabolized in the liver
  2. inorganic fluoride ions are liberated
  3. Fluoride ions are nephrotoxic
231
Q

How doe fluoride ions affect renal function

A

They impair the concentrating mechanism in the renal tubules

232
Q

What is the etiology of aminoglycosides on AKI

A

These drugs are polycationic compounds that bind to anionic brush border in proximal tubule

The compounds are transported into the cytosol where they induce free radical change

233
Q

List antibiotics that can induce renal injury

A
  1. aminoglycosides
  2. amphotericin B
  3. vancomycin
  4. sulfonamides
  5. tetracyclines
  6. cephalosporins
234
Q

What are calcineurin inhibitors

Renal effects

A

Cyclosporine and Tacrolimus
Immunosuppressants to prevent transplant rejection

Effects = HTN and renal vasoconstriction

235
Q

What 5 conditions can cause rhabdomyolysis and myoglobinemia

A
  1. Direct muscle trauma
  2. Muscle ischemia
  3. Prolonged immobilization
  4. MH
  5. Succinylcholine in pts w/ Duchenne MD
236
Q

Most common anesthetic method for TURP and why

A

Neuraxial with a T10 level

To be able to assess pts neurologic status during procedure

237
Q

How do irrigation fluids used during TURP affect circulation

A

A portion of fluid is absorbed via prostate venous sinuses and enters circulation

238
Q

What risks are associated with the continuous irrigation during TURP

A

Systemic volume overload

Toxicity from irrigation solution

239
Q

What is the estimated absorption of irrigation fluid during TURP

A

~10-30 mL/min of resection time

240
Q

How does the height of irrigation fluid during TURP affect systemic volume

A

Solution should be less than 60 cm above OR table

Height should be lowered towards the end b/c more prostate venous sinuses are open to absorb irrigation

241
Q

Reasoning for NOT using LR or 0.9% NaCl during TURP

A

They are highly ionized and good conductors of electricity

Contraindicated when monopolar electrocautery is used

242
Q

What are the cons of using distilled water with TURP irrigation

A
  1. Decreased serum osmolarity causing
    a. dilutional hyponatremia
    b. hemolysis
243
Q 
Osmolarity of the following irrigation solutions
Distilled water=
Glycine=
Sorbitol 3.3%=
Mannitol 5%=
NaCl 0.9%=
A 
mOsm/L
Distilled water= 0
Glycine= 200
Sorbitol 3.3%= 165
Mannitol 5%= 275
NaCl 0.9%= 308
244
Q 
What are the benefits of the following irrigation solutions
Distilled water=
Glycine=
Sorbitol 3.3%=
Mannitol 5%=
NaCl 0.9%=
A

Distilled water= good visibility
Glycine= decreased risk of TURP syndrome
Sorbitol 3.3%= Decreased risk of TURP syndrome
Mannitol 5%= Osmo similar to plasma, renal filtration and excretion
NaCl 0.9%= Osmo slightly higher than plasma, decreased side effects

245
Q

What are cons for using distilled water for TURP

A

Increased risk of TURP syndrome

  • Hyponatremia
  • Hemolysis
  • Hemoglobinuria = renal failure
246
Q

What are the cons of using glycine irrigation during TURP

A
  1. Increased ammonia = decreased LOC
  2. Transient postop visual syndrome
    - blindness, blurry vision for 24-48 hrs
    - inhibitory NT in the eye
247
Q

What are the cons of sorbitol 3.3% irrigation during TURP

A
  1. Hyperglycemia
  2. Osmotic diuresis
  3. Lactic acidosis (w/ massive absorption)
248
Q

What are the cons of mannitol 5% irrigation during TURP

A
  1. Osmotic diuresis

2. Transient plasma expansion and risk for LV failure

249
Q

What are the cons of NaCl 0.9% irrigation during TURP

A
  1. Can only be used w/ bipolar cautery

2. Contraindicated w/ monopolar cautery

250
Q

What causes TURP syndrome

A

Large volume of hypo-osmolar irrigation solution

251
Q

What is the classic triad of TURP syndrome symptoms

A
  1. HTN (w/ increased pulse pressure)
  2. Bradycardia (reflexive)
  3. Mental status change
252
Q

How does serum Na+ level affect TURP syndrome

A

Na+ < 120 mEq/L increases risk of complications

Na+ <110 mEq/L associated w/ Sz, coma, lethal ventricular dysrhythmias

253
Q

What are 5 CNS symptoms of TURP syndrome

A
  1. Restlessness
  2. N/V
  3. Cerebral edema
  4. Sz
  5. Coma
254
Q

What is the treatment of TURP syndrome

A
  1. Support oxygenation and CV
  2. Tell surgeon to abort
  3. Labs (lytes, hct, crt, glucose, 12 lead)
  4. give fluids based on serum Na+
  5. Avoid rapid Na+ correction
  6. Midazolam for Sz
  7. Intubation if oxygenation is compromised
255
Q

How should fluid replacement be directed by Na+ level

A

Na+ > 120 = restrict fluids and give loop diuretic

Na <120 = give 3% NaCl at 100 ml/hr

256
Q

What can result from correcting Na+ too quickly

A

Central pontine myelinolysis

257
Q

What are 3 complication associated with TURP (not TURP syndrome)

A
  1. Bladder perforation
  2. Bleeding
  3. Hypothermia
258
Q

What are factors that can lead to bladder perforation

A

Resectoscope punctures bladder wall

Stimulation of obturator nerve through bladder causing extremity movement

259
Q

What are symptoms of bladder perforation

A

abdominal and shoulder pain

260
Q

What is an early sign of bladder rupture

A

Decreased return of irrigation fluid

261
Q

What is the resulting treatment of bladder perforation

A

emergent suprapubic cystostomy or ex-lap

262
Q

How is EBL affected by TURP

A

accurate estimation is difficult d/t irrigation fluid

EBL ~2-5 mL/min of resection time

263
Q

How does extracorporeal shock wave lithotripsy work

A

Delivers shock wave in rapid succession at the stone
The shock wave moves through water and tissue until it reaches the stone
Stone is broken into fragments to pass with urine

264
Q

What are 2 absolute contraindications for ESWL

A
  1. Pregnancy

2. Risk of bleeding (on anticoag)

265
Q

What are 5 relative contraindications for ESWL

A
  1. PM/ICD
  2. Calcified aortic aneurysm or renal artery
  3. UTI untreated
  4. Obstruction beyond stone preventing elimination
  5. Morbid obesity (increased distance from energy)
266
Q

What are complications of ESWL

A
  1. Shock can produce dysrhythmias
  2. Organ perforation
  3. Skin bruising
  4. Hematuria
267
Q

How is dysrhythmia prevent with ESWL

A

Synchronize shock w/ R wave to prevent R-on-T phenomena

268
Q

What is the procedure for percutaneous nephrolithotripsy

A
  1. Urethral stent

2. Nephrostomy tube for stone retrieval

269
Q

Anesthetic type and possible positioning for percutaneous nephrolithotripsy

A

GETA

Prone

270
Q

What are possible complications of percutaneous nephrolithotripsy

A

Complication r/t irrigation fluid (same as TURP)

APEX-KLE (4 decks)

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