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KLE-Kidney Flashcards

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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
What percentage of the blood delivered to the kidneys is processed by the glomerulus vs circulated via peritubular capillaries
20% via glomerulus | 80% via peritubular capillaries
26
What percent of the ultrafiltrate, originally from glomerular filtration, is reabsorbed
99%
27
What is the distribution of blood flow to the following portions of the kidney: Cortex Medulla/juxtamedullary nephron
Cortex = 90% | Medulla/juxtamedullary nephron = 10%
28
What is the PaO2 in the following portions of the kidneys: Cortex Medulla/juxtamedullary nephron
Cortex = 50 mmHg | Medulla/juxtamedullary nephron = 10 mmHg
29
Why is the renal medulla more sensitive to ischemia
Because the PaO2 is ~10 mmHg
30
How does renal blood flow change during the life-span
It decreases 10% per decade of life after 50-years
31
Equation for renal blood flow
RBF = (MAP - renal venous pressure) / renal vascular resistance
32
Describe the arterial renal blood flow starting at the renal artery
renal a. => interlobar a. => arcuate a. => interlobular a. => afferent aa => glomerular capillary bed => efferent aa => peritubular capillary beds
33
Describe the venous renal blood flow starting at the peritubular capillary bed
Peritubular cap bed => venules => interlobular v => arcuate v => interlobar v => renal segmental v => renal vein
34
What is glomerular filtration dependent on when MAP is outside of the range of autoregulation
Glomerular filtration becomes pressure dependent
35
How does autoregulation of the kidneys affect renal perfusion
Low perfusion = autoreg increases RBF by decreasing renal vascular resistance High perfusion = decrease RBF by increasing renal vascular resistance
36
What are 6 processes that aid in renal autoregulation
1. Myogenic mechanism* 2. Juxtaglomerular apparatus and tubuloglomerular feedback* 3. RAAS 4. Prostaglandins 5. Atrial natriuretic peptide 6. SNS
37
Describe the impact of myogenic mechanisms on renal autoregulation
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
38
Where is the juxtaglomerular apparatus located
Distal tubule in the region that passes between the afferent and efferent aa.
39
What is the mechanism by which the tubuloglomerular feedback system autoregulates renal blood flow
It gains feedback about Na+ and Cl- composition in the distal tubule affecting arteriolar tone This creates a negative feedback loop to maintain RBF
40
Where do the kidneys receive SNS innervation
T8-L1
41
How does the SNS impact RBF during the perioperative period | What is the kidney at increased risk for
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
42
What renal structures are innervated by the SNS
Afferent and efferent aa
43
What change alerts the juxtaglomerular apparatus to decreased RBF What is the response
Decreased GFR reduces Na+ and Cl- delivery | The afferent aa is then dilated to restore GFR
44
What structure senses alterations in Na+ and Cl- concentrations in the juxtaglomerular apparatus
The macula densa
45
When low Cl- concentration is detected by the macula densa, what is the response
Renin release from the JG cells, this activates the RAAS Ang 2 constricts the efferent aa, increasing GFR
46
What 2 JGA mechanisms increase GFR
Dilation of afferent aa when Na/Cl delivery is reduced Constriction of efferent aa when Cl- concentration is low
47
What is the relationship of urine output and MAP
The relationship is linear UO typically halts when MAP<50 mmHg UO is NOT auto-regulated
48
What are 3 conditions that stimulate renin release
1. Beta-1 stimulation (SNS activation) 2. Hypovolemia (decreased renal perfusion) 3. Hyponatremia (tubuloglomerular feedback)
49
Describe the RAAS
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
50
How does angiotensin II affect BP
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
51
What are causes of decreased renal perfusion pressure that can increase renin release
1. Hemorrhage 2. PEEP 3. CHF 4. Liver failure w/ ascites 5. Sepsis 6. Diuresis
52
Where is aldosterone produced
Zona glomerulosa of the adrenal gland
53
What 2 action does aldosterone have in the kidneys
1. Stimulates Na/K-ATPase in principal cells of distal tubules and collecting ducts 2. Facilitates Na+ and H2O reabsorption and K+/H+ excretion
54
What 2 electrolyte imbalances can stimulate aldosterone release
1. Hyperkalemia | 2. Hyponatremia
55
What is Conn's disease
Disease of excess aldosterone production | Causes Na+ retention and K+ loss
56
Stimulation of which adrenergic receptor increases renin release
Beta-1
57
Where is ADH produced
Hypothalamus (supraoptic and paraventricular nuclei)
58
Where is ADH released
Posterior pituitary gland
59
What are 2 other names for ADH
Vasopressin | Arginine vasopressin
60
What are the 2 mechanisms that control ADH release
1. Increased osmolarity of ECF | 2. Decreased blood volume
61
How does an increased osmolarity trigger ADH release
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)
62
How does decreased blood volume trigger ADH release
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
63
How does ADH restore blood volume
1. Stimulates V1 receptor causing vasoconstriction of peripheral vasculature and increasing IP3 2. Stimulates V2 receptor in collecting ducts, increasing cAMP
64
How does ADH cause vasoconstriction
Stimulates V1 receptors in periphery. This increases IP3, DAG, and Ca++ leading to vasoconstriction
65
What anesthetic effects can increase ADH release
1. PEEP 2. PPV 3. HoTN 4. Hemorrhage (anything that affects arterial BP or venous blood return decreasing CO)
66
How does ADH facilitate water reabsorption and affect osmolarity
It upregulates aquaporin-2 channels in the collecting ducts (medulla) This increased water reabsorption (w/o Na+), reducing plasma osmolarity and increasing urine osmolarity
67
What is the physiologic response of the V1 and V2 receptors
``` V1 = peripheral vasoconstriction V2 = expansion of plasma volume via H2O reabsorption in kidneys ```
68
What are 3 mechanisms that promote renal vasodilation
1. Prostaglandins 2. Natriuretic peptide 3. Dopamine receptors
69
What is the role of prostaglandins in the kidneys
Promoting renal blood flow following production in the afferent aa.
70
Why do NSAIDs impact renal blood flow
They block cyclooxygenase which ultimately inhibits renal prostaglandin vasodilatory effects
71
What mediators are produced by the myocardium in response to atrial distension
Atrial and brain natriuretic peptide
72
What is the role of natriuretic peptides
1. Inhibit renin release (negative feedback on RAAS) | 2. Promote Na+ and H2O excretion into collecting ducts
73
What dopamine receptors are present in the kidneys
DA1
74
What is the location and 2nd messenger of DA1 receptors
Location = renal vasculature, tubules 2nd messenger = Increased cAMP
75
What is the role of DA1 receptors in the kidney
1. Vasodilation 2. Increased RBF 3. Increased GFR 4. Diuresis 5. Na+ excretion
76
What is the MOA and class of fenoldopam
``` Class = DA1 receptor agonist MOA = increases renal blood flow via renal vasodilation, increased GFR, and Na+ excretion ```
77
What are the portions of the nephron starting at the glomerulus
Glomerulus => Bowman's capsule => proximal convoluted tubule => loop of Henle (descending loop ==> ascending loop thin/thick) => Distal convoluted tubule => collecting duct
78
What is the normal GFR Glomerular filtration fraction
GFR = 125 mL/min | Filtration fraction = 20%
79
What substances are freely filtered at the glomerulus. | What substances are not
Filtered = Water, electrolytes and glucose | Not filtered = plasma proteins (albumin)
80
How does the glomerular filtrate differ from plasma
It does not contain plasma proteins, erythrocytes, or WBCs
81
What does kidney disease destroy
The basement membrane allowing proteins to enter the tubules
82
How is the net filtration pressure of the nephron determined
NFP = glomerular hydrostatic P - Bowman's capsule hydrostatic P - Glomerular oncotic P
83
What factor is the most important determinant of GFR
Glomerular hydrostatic pressure
84
What are the 3 factors that determine glomerular hydrostatic pressure
1. Arterial BP 2. Afferent arteriole resistance 3. Efferent arteriole resistance
85
How does arterial BP affect GFR
increased MAP = increased GFR | Decreased MAP = decreased GFR
86
How is the kidney protected from hypo-hyperperfusion
Autoregulation, as long as the BP are within the upper and lower limits
87
How does afferent aa resistance affect GFR
``` Constriction = decreased GFR Dilation = increased GFR ```
88
How does efferent aa resistance affect GFR
Constriction: - mild = decreased peritubular flow, increased GFR - Excessive = reduced RBF and GFR Dilation = increases peritubular flow and decreases GFR
89
Define the following in terms of renal physiology Reabsorption Secretion Excretion
Reabsorption = from tubule (pee) to peritubular capillaries (circ) Secretion = form peritubular capillaries (circ) to tubules (pee) Excretion = removed from body in urine
90
What is the equation of urine production
Urinary excretion rate = filtration - reabsorption + secretion
91
What is the primary function of the PCT
Bulk reabsorption of solutes and water
92
Where does the most Na+ get reabsorbed in the nephron
The PCT (65%)
93
What ions are reabsorbed in bulk at the PCT and how
Active transport: Na+ Na+ Co-transport: K+ Cl- HCO3
94
What substances are secreted into the PCT via Na+ counter-transport
Organic bases Acids H+
95
What organic acids and bases are exchanged for Na+ counter-transport in the PCT
``` Bile salts Uric acid Catecholamines Toxins Some drugs ```
96
What is the primary function of the descending loop of Henle
Forming concentrate or dilute urine via separation of Na+ and H2O handling
97
What is the function of the vasa recta
To maintain the medullary osmotic gradient | Vasa recta is the vasculature surrounding the loop of Henle
98
What are the 2 countercurrent systems that maintain the hyperosmotic peritubular insterstium
Loop of Henle = creates the gradient Vasa recta = maintains the medullary osmotic gradient
99
Describe the permeability of the descending limb of the loop of Henle
Highly permeable to water (20% of H2O reabsorption occurs here) Modestly permeable to ions
100
What happens to osmolarity along the descending loop of Henle
It increases from 300 to 1500 at the renal pelvis
101
Describe the permeability of the ascending loop of Henle
The thin and thick segments are NOT permeable to water
102
What is the most important ion pump in the ascending loop of Henle
The Na-K-Cl cotransporter | Pumps ions from tubular fluid into peritubular interstitum
103
What section of the nephron is the target of loop diuretics
The ascending loop, Na-K-Cl cotransporter
104
Where is the second greatest site of Na+ reabsorption
The ascending loop (via Na-K-Cl cotransporter)
105
What ion is excreted in the ascending tubule via what mechanism
H+ via the Na-H exchange mechanism
106
What actions occur in the distal convoluted tubule
Fine tuning of solute concentration | -5% of Na+ is reabsorbed (along with K, Cl, HCO3 via co-transport)
107
Which sections of the nephron are impermeable to H2O
1. Ascending loop | 2. Late distal tubule (except w/ aldosterone or ADH)
108
Which portion of the nephron do aldosterone and ADH act
The DCT and collecting duct
109
What portion of the nephron does PTH influence Ca++ reabsorption
DCT
110
What portion of the nephron does atrial natriuretic peptide act
Collecting duct
111
What are actions that occur at the collecting duct
1. Reabsorb 5% of Na+ 2. ADH and aldosterone action 3. ANP inhibits water/Na+ reabsorption 4. Adjusts H+ concentration
112
Where is the site of action of acetazolamide | MOA
The proximal tubule | MOA = Carbonic anhydrase is inhibited, reducing HCO3-, Na+ and H2O reabsorption
113
What are 3 clinical uses of acetazolamide
1. Open-angle glaucoma 2. High altitude sickness 3. Central sleep apnea
114
What are complications of acetazolamide use
1. Metabolic acidosis 2. Hypokalemia 3. Exacerbated CNS depression in COPD (d/t loss of HCO3
115
What is the site and mechanism of action for osmotic diuretics in the nephron
They undergo filtration but not reabsorption Inhibition of water reabsorption in the PCT and loop of Henle
116
What is the site and mechanism of action of loop diuretics | Examples
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
What ions are lost with loop diuretic use
Na, K, Ca, Mg, Cl
118
What is the site and mechanism of action of thiazide diuretics Examples
``` 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
What is a unique side effect of thiazide diuretics
They can cause hyperglycemia
120
What type of a acid-base disturbance can result from thiazide and loop diuretics
Hypokalemic, hypochloremic metabolic alkalosis
121
Metabolic acidosis can be the result of what kind of diuretic use
Carbonic anhydrase inhibitor (acetazolamide) | Potassium-Sparing diuretics
122
What is the site and mechanism of action of potassium-sparing diuretics Examples
Site = Collecting ducts MOA = inhibition of K+ secretion and Na+ reabsorption
123
How does spironolactone differ from other potassium-sparing diuretics
It is an aldosterone antagonists | Blocking aldosterone at mineralocorticoid receptors, inhibiting K secretion and Na+ reabsorption
124
What are 2 reasons amiloride is administered
1. To reduce K+ loss in a patient receiving a loop or thiazide diuretics 2. Secondary hyperaldosteronism
125
5 Side effects of potassium-sparing diuretics
1. Hyperkalemia 2. Metabolic acidosis 3. Gynecomastia 4. Libido changes 5. Nephrolithiasis
126
What are 3 drug classes that increase the risk of hyperkalemia in a patient on potassium-sparing diuretics
1. NSAIDs 2. Beta-blockers 3. ACE inhibitors
127
What 2 functions are assessed with renal function tests
1. Glomerular function | 2. Tubular function (concentrating ability)
128
Which tests assess glomerular function
Blood urea nitrogen Serum Creatinine Creatinine clearance
129
Which tests assess tubular function (concentrating ability)
``` TESTS ON URINE Fractional excretion of Na+ Urine osmolality Urine Na+ concentration Urine specific gravity ```
130
What does a low BUN indicate
1. Overhydration | 2. Decreased urea production (malnutrition or liver dz)
131
What does can an elevated BUN indicate
1. Dehydration 2. Increased protein input (GIB, hematoma breakdown) 3. Catabolism (Trauma, sepsis) 4. Decreased GFR
132
What is creatinine
A metabolic byproduct of creatin breakdown which is produced by skeletal muscle
133
Why is BUN a better indicator of uremic symptoms than a measure of GFR
B/c it underdoes filtration and reabsorption
134
Why is creatinine a better indicator of GFR
It undergoes filtration only (no reabsorption)
135
What does a 100% increase in creatinine indicate for the GFR
a 50% reduction
136
What is the significance of BUN:crt ratio
Helps evaluate the state of hydration
137
What do the following BUN:creatinine values indicate 10:1 = >20:1 =
``` 10:1 = normal ratio >20:1 = prerenal azotemia (increased nitrogen compounds) ```
138
What is the most useful indicator of GFR
Creatinine clearance
139
What do the following values of Fractional excretion of Na+ indicate Fe(Na+) <1% Fe(Na+) >3%
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
What is the significance of fractional excretion of Na
It relates Na+ clearance to creatinine clearance
141
What does an elevated urine sodium indicate
Failing kidneys | Kidney failure wastes Na+
142
What is the most common cause of perioperative kidney injury
ischemia-reperfusion injury
143
What patient characteristics increase the risk of perioperative AKI
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
What is the common cause of oliguria in the perioperative period
prerenal origin
145
Why is urine output not a reliable surrogate for perioperative renal perfusion
Because perioperative stress increases ADH release which causes H2O and Na+ reabsorption
146
What are the classes of renal injury considered with the RIFLE criteria
``` Risk Injury Failure Loss End-Stage ```
147
What are the criteria for renal injury RIFLE classes
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
What are the stages of the AKIN classification of renal injury
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
What are 5 causes of prerenal injury
Hypoperfusion d/t: 1. Hypovolemia 2. Decreased CO 3. Systemic vasodilation 4. Renal vasoconstriction 5. Increased intra-abd pressure
150
What is treatment for prerenal injury
1. Restoration of RBF w/ IVF, PRBCs, and hemodynamic support | 2. Renal prostaglandins for vasodilation. Avoid NSAIDs
151
How can treatment for prerenal injury be diagnoses
Improvement in UOP following IVF bolus
152
What is the cause of intrinsic kidney injury
Parenchymal damage
153
What does 80% of the O2 delivered to the kidney feul
Ionic gradients in the nephron
154
What section of the kidney is injured with intrinsic renal damage
Medulla d/t medullary ischemia
155
What are intrinsic causes of acute tubular necrosis
1. Ischemia | 2. Nephrotoxic drugs
156
What are factors that increase intrinsic renal injury
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
What is the treatment for intrinsic kidney injury
1. Restore renal perfusion | 2. Supportive
158
What is the cause of postrenal injury Treatment
Obstruction between collecting system and urethra Treatment = relieve obstruction
159
5 factors that increase prerenal injury
1. Intravascular volume depletion 2. Decreased CO 3. Systemic vasodilation 4. Renal vasoconstriction 5. Increased abd pressure
160
What are 5 factors that increase intrinsic renal injury
1. Tubular injury 2. Tubulointerstitial injury 3. Glomerular injury 4. Renal vasculature 5. Large vessels
161
What are 6 factors that contribute to tubular injury
1. Ischemia from hypoperfusion 2. Myoglobin 3. Free hgb (transfusion rxn) 4. Antibiotics 5. Contrast agents 6. Chemotherapeutics
162
What are 3 factors that contribute to tubulointerstitial injury
1. Acute allergic interstitial nephritis 2. Infection 3. Infiltration
163
What are 3 factors that contribute to glomerular injury
1. Inflammatory dz 2. Hemolytic uremic syndrome 3. Thrombotic thrombocytopenic purpura
164
What are 4 factors that contribute to renal vasculature issues and intrinsic renal injury
1. Toxemia of pregnancy 2. Hypercalcemia 3. Contrast agents 4. MH 5. Scleroderma
165
What are 4 factors that contribute to large vessel issues causing intrinsic kidney injury
1. Thrombosis 2. Vasculitis 3. Dissection 4. Trauma
166
How can prerenal azotemia be reduced
1. Maintain MAP>65 mmHg | 2. Hydration
167
What type of fluid can increase risk of renal morbidity
Fluids containing hydroxyethyl starches
168
What acid base imbalance is caused by excessive o.9% NaCl
Hyperchloremic metabolic acidosis
169
How can diuretic use impact renal health in AKI
Attempting to convert oliguric to nonoliguric AKI can increase the risk of additional renal injury
170
How do alpha-1 agonists impact RBF in healthy vs septic pts
1. Healthy pts can have reduced RBF 2. Septic pts can benefit if MAP is supported - Renal perfusion outweigh renal vasoconstrictive effects
171
How does vasopressin use affect RBF
1. Preferentially constricts efferent arteriole | 2. Maintains GFR and UOP
172
How does dopamine affect renal perfusion
Renal dose of dopamine does not prevent or treat AKI
173
What nephrotoxic drugs should be avoided in pts at risk for AKI
1. Aminoglycoside abx 2. Amphotericin B 3. NSAIDs 4. Diuretics unless pt is fluid overloaded
174
``` What is the type and GFR associated with the following stages of kidney disease 1 2 3 4 5 ```
``` 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
What are s/sx of uremic syndrome
1. Anemia 2. Fatigue 3. N/V 4. Anorexia 5. Coagulopathy
176
How is BUN level associated with uremic symptoms
It parallels symptoms and can guide management
177
How is bleeding affected by uremia
1. Increase risk of bleeding | 2. Bleeding time is increased
178
How are coagulation tests affected by uremia
PT, PTT, and plt counts are normal | Bleeding time is increased
179
How is increased bleeding time treated with uremia
Desmopressin is first-line treatment
180
What treatment can improve bleeding time in uremic pts
1. Desmopressin | 2. Dialysis
181
What type of anemia do CKD pts have
Normochromic normocytic anemia from decreased erythropoietin production
182
What is the treatment for CKD associated anemia
Exogenous EPO or darbepoetin iron supplementation
183
Why is blood transfusion not a first-line treatment for CKD related anemia
It increases the risk of HLA sensitization increasing the risk for future rejection of transplanted kidney
184
What is the cause of ckd related HTN
RAAS activation leading to sodium retention and fluid overload
185
What are CV effects of CKD and their cause
``` Effects = CHF, pulm edema Cause = Na+ and H2O retention ```
186
What is the most common cause of death in CKD pts
CAD, assume all CKD pts have CAD
187
What cardiac pathology is common with uremia
Pericarditis is common Risk for pericardial effusion and cardiac tamponade
188
What is the etiology of acid-base imbalance in CKD
decreased excretion of non-volatile acid Contributes to gap metabolic acidosis from accumulation of non-volatile acids
189
How does acidosis in CKD affect the oxyhgb dissociation curve
Shift right Partially compensates for anemia
190
What is the etiology of hyperkalemia in CKD | When is dialysis indicated
D/t impaired K excretion Dialysis when K> 6 mEq//L
191
What are additional treatments for hyperkalemia
1. Glucose (25-50 g)+ insulin (10 - 20 units) 2. hyperventilate 3. NaHCO3 50 - 100 mEq
192
How does hyperventilation affect serum K
For every 10 mmHg in PaCO2 serum K decreases by 0.5 mEq/L
193
Why is CaCl (1 g) given with elevated serum K
It raises the threshold potential reducing the risk of lethal dysrhythmias
194
How does CKD affect skeletal structure
Causes osteodystrophy
195
What is the cause of renal osteodystrophy
1. Decreased vitamin D production | 2. Secondary hyperparathyroidism
196
What is the pathophysiology of CKD associated Vit D under production and osteodystrophy
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
How is phosphate level associated with CKD
It is elevated which contributes to low serum Ca++ Phosphate clearance is inversely proportion to GFR low GFR = HI phosphate
198
What respiratory pattern is a result of uremia
Increased intravascular volume creates restrictive ventilatory defect
199
Respiratory effects of CKD
1. Restrictive ventilatory defect 2. Pulmonary edema 3. Hyperventilation d/t respiratory compensation of met acidosis
200
What is a neurologic effect of uremia
1. Impaired nerve conduction 2. Peripheral neuropathy 3. Autonomic dysfunction
201
Result of autonomic dysfunction d/t CKD
Contributes to reduce baroreceptor responsiveness | Delays gastric emptying
202
What is the risk of peripheral neuropathy in the CKD pt
Since it is both sensory and motor, this contributes to silent MI
203
How does CKD affect risk for infection
Impaired WBC function and low protein diets contribute to the high risk of infection Blood products increase risk of viral transmission
204
What are the 5 indications for dialysis in CKD
1. Volume overload 2. Hyperkalemia 3. Sever metabolic acidosis 4. Symptomatic uremia 5. OD w/ drugs that are cleared renally
205
What are 5 reasons anesthetic drugs have altered response in CKD
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
What are 3 exaggerated hemodynamic effects associated with altered anesthetic drug action in CKD
1. Antihypertensive medications especially ACE-i and ARBs 2. Attenuation of SNS tone 3. PPV
207
How do halogenated anesthetics contribute to AKI
They can reduce renal perfusion (systemic vasodilation) coupled with renal vasoconstriction from vasopressors and injury from nephrotoxic agents
208
Is succinylcholine safe to use in renal failure
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
Why should succinylcholine infusion be avoided in renal disease
The primary metabolite (succinylmonocholine) is excreted by the kidneys, so paralysis may be prolonged d/t its weak action
210
Which NMB drugs are most appropriate in renal failure and why
Benzylisoquinolines (cisatracurium and atracurium) Organ independent elimination
211
What are causes of the potential for rocuronium increased duration of action
1. reduced clearance 2. altered protein binding 3. increased potency
212
Which aminosteroids are safe for use in renal failure
Rocuronium is most appropriate Vec and Panc should not be used
213
Why should vecuronium and pancuronium be avoided in renal failure
Vec = 3-OH vecuronium metabolite increased duration of action d/t decreased clearance and increase elim HL Panc = primarily eliminated by kidneys
214
What effects does renal disease have on reversal agents
1. anticholinesterases and anticholinergics undergo renal elimination and can have increased duration 2. Sugammadex is not recommended in pts with severe renal impairment
215
Which opioids should be avoided in renal disease
1. Morphine | 2. Meperidine
216
Why should morphine be avoided in renal disease
The active metabolite (morphine-6-glucuronide) i smore potent than morphine and relies on renal excretion Accumulation can cause respiratory depression
217
Why should meperidine be avoided in renal disease
It is metabolized into normeperidine | Accumulation of the metabolite can cause convulsions
218
Which opioids are safe to use in renal disease
1. Fentanyl 2. Sufentanil 3. alfentanil 4. remifentanil 5. hydromorphone (controversial potential metabolite)
219
What are 4 factors that accelerate compound A production with Sevo use
1. High concentration for prolong time 2. Low FGF 3. Hi temp of CO2 absorbent 4. Increased CO2 production
220
How does radiographic contrast media cause nephrotoxicity
1. Ischemic injury d/t vasoconstriction in renal medulla | 2. Direct cytotoxic effect
221
What are 6 methods to prevent contrast-induced nephropathy
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
How does N-acetylcysteine impact contrast-induced nephropathy
It is a free radical scavenger but has been determined to be less efficacious
223
How does increased myoglobin impact the kidneys
It can precipitate in the proximal tubules causing tubular obstruction and ATN
224
Why does myoglobin cause ATN
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
How does myoglobin cause vasoconstriction
It scavenges NO leading to renal vasoconstriction and ischemia
226
What wastes are released during rhabdomyolysis that can cause kidney injury
1. Myoglobin | 2. Creatine phosphokinase
227
What are AKI preventative strategies during rhabdomyolysis
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
What medications are given to the pt w/ rhabdomyolysis
1. Mannitol 2. NaHCO3 3. Acetazolamide
229
How does sevoflurane impair renal function
1. Compound A | 2. Free fluoride ions
230
How does sevo metabolism affect renal function
1. 5% of sevo is metabolized in the liver 2. inorganic fluoride ions are liberated 3. Fluoride ions are nephrotoxic
231
How doe fluoride ions affect renal function
They impair the concentrating mechanism in the renal tubules
232
What is the etiology of aminoglycosides on AKI
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
List antibiotics that can induce renal injury
1. aminoglycosides 2. amphotericin B 3. vancomycin 4. sulfonamides 5. tetracyclines 6. cephalosporins
234
What are calcineurin inhibitors | Renal effects
Cyclosporine and Tacrolimus Immunosuppressants to prevent transplant rejection Effects = HTN and renal vasoconstriction
235
What 5 conditions can cause rhabdomyolysis and myoglobinemia
1. Direct muscle trauma 2. Muscle ischemia 3. Prolonged immobilization 4. MH 5. Succinylcholine in pts w/ Duchenne MD
236
Most common anesthetic method for TURP and why
Neuraxial with a T10 level | To be able to assess pts neurologic status during procedure
237
How do irrigation fluids used during TURP affect circulation
A portion of fluid is absorbed via prostate venous sinuses and enters circulation
238
What risks are associated with the continuous irrigation during TURP
Systemic volume overload | Toxicity from irrigation solution
239
What is the estimated absorption of irrigation fluid during TURP
~10-30 mL/min of resection time
240
How does the height of irrigation fluid during TURP affect systemic volume
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
Reasoning for NOT using LR or 0.9% NaCl during TURP
They are highly ionized and good conductors of electricity | Contraindicated when monopolar electrocautery is used
242
What are the cons of using distilled water with TURP irrigation
1. Decreased serum osmolarity causing a. dilutional hyponatremia b. hemolysis
243
``` Osmolarity of the following irrigation solutions Distilled water= Glycine= Sorbitol 3.3%= Mannitol 5%= NaCl 0.9%= ```
``` mOsm/L Distilled water= 0 Glycine= 200 Sorbitol 3.3%= 165 Mannitol 5%= 275 NaCl 0.9%= 308 ```
244
``` What are the benefits of the following irrigation solutions Distilled water= Glycine= Sorbitol 3.3%= Mannitol 5%= NaCl 0.9%= ```
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
What are cons for using distilled water for TURP
Increased risk of TURP syndrome - Hyponatremia - Hemolysis - Hemoglobinuria = renal failure
246
What are the cons of using glycine irrigation during TURP
1. Increased ammonia = decreased LOC 2. Transient postop visual syndrome - blindness, blurry vision for 24-48 hrs - inhibitory NT in the eye
247
What are the cons of sorbitol 3.3% irrigation during TURP
1. Hyperglycemia 2. Osmotic diuresis 3. Lactic acidosis (w/ massive absorption)
248
What are the cons of mannitol 5% irrigation during TURP
1. Osmotic diuresis | 2. Transient plasma expansion and risk for LV failure
249
What are the cons of NaCl 0.9% irrigation during TURP
1. Can only be used w/ bipolar cautery | 2. Contraindicated w/ monopolar cautery
250
What causes TURP syndrome
Large volume of hypo-osmolar irrigation solution
251
What is the classic triad of TURP syndrome symptoms
1. HTN (w/ increased pulse pressure) 2. Bradycardia (reflexive) 3. Mental status change
252
How does serum Na+ level affect TURP syndrome
Na+ < 120 mEq/L increases risk of complications Na+ <110 mEq/L associated w/ Sz, coma, lethal ventricular dysrhythmias
253
What are 5 CNS symptoms of TURP syndrome
1. Restlessness 2. N/V 3. Cerebral edema 4. Sz 5. Coma
254
What is the treatment of TURP syndrome
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
How should fluid replacement be directed by Na+ level
Na+ > 120 = restrict fluids and give loop diuretic Na <120 = give 3% NaCl at 100 ml/hr
256
What can result from correcting Na+ too quickly
Central pontine myelinolysis
257
What are 3 complication associated with TURP (not TURP syndrome)
1. Bladder perforation 2. Bleeding 3. Hypothermia
258
What are factors that can lead to bladder perforation
Resectoscope punctures bladder wall Stimulation of obturator nerve through bladder causing extremity movement
259
What are symptoms of bladder perforation
abdominal and shoulder pain
260
What is an early sign of bladder rupture
Decreased return of irrigation fluid
261
What is the resulting treatment of bladder perforation
emergent suprapubic cystostomy or ex-lap
262
How is EBL affected by TURP
accurate estimation is difficult d/t irrigation fluid EBL ~2-5 mL/min of resection time
263
How does extracorporeal shock wave lithotripsy work
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
What are 2 absolute contraindications for ESWL
1. Pregnancy | 2. Risk of bleeding (on anticoag)
265
What are 5 relative contraindications for ESWL
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
What are complications of ESWL
1. Shock can produce dysrhythmias 2. Organ perforation 3. Skin bruising 4. Hematuria
267
How is dysrhythmia prevent with ESWL
Synchronize shock w/ R wave to prevent R-on-T phenomena
268
What is the procedure for percutaneous nephrolithotripsy
1. Urethral stent | 2. Nephrostomy tube for stone retrieval
269
Anesthetic type and possible positioning for percutaneous nephrolithotripsy
GETA | Prone
270
What are possible complications of percutaneous nephrolithotripsy
Complication r/t irrigation fluid (same as TURP)

APEX-KLE (4 decks)

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