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N935 Advanced Pathophysiology > Week 5 Renal Pathophysiology > Flashcards

Week 5 Renal Pathophysiology Flashcards

1
Q

What percent do the kidneys receive of total cardiac output?

A

15-25%

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2
Q

How much is directed to renal cortex?

A

95%

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3
Q

How much is directed to medulla?

A

5%

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4
Q

How much blood flows through the renal arteries?

A

1-1.25L/min

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5
Q

What is more vulnerable to ischemic insults?

A

renal medullary papillae

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6
Q

what mean arterial pressures does the kidney successful autoregulate their blood flow?

A

60-160mmHg

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7
Q

What causes vasodilation and vasoconstriction of renal afferent arterioles and regulates the autoregulation of RBF?

A

intrinsic mechanism

innervation intact even in denervated kidneys

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8
Q

What is the purpose of the glomerulus?

A

separates the afferent arterioles from the efferent arterioles

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9
Q

What does the resistance in the efferent arterioles create?

A

hydrostatic pressure within the glomerulus to provide force for ultrafiltration

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10
Q

What are the capillaries lined with endothelial cells called?

A

podocytes

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11
Q

Glomerular filtration rate is

A

the rate at which blood is filtered through all of the glomeruli measure overall kidney function

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12
Q

SNS activation does what to renal blood flow?

A

reduces renal blood flow

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13
Q

Example of SNS activation and RBF:

A

shunt to skeletal muscle during exercise
surgical stimulation can increase vascular resistance
stimulates the adrenal medulla-> catecholamine release
if BP decreases SNS will also stimulate RASS

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14
Q

Antidiuretic hormone is released in response to

A

DECREASED stretch receptors in the atrial and arterial wall

Increased osmolality of the plasma (monitored by hypothalamus)

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15
Q

Where is ADH synthesized?

A

hypothalamus and is released from the posterior pituitary

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16
Q

what is the half life of ADH

A

16-24 minutes

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17
Q

What are the two primary functions of ADH

A

increases reabsorption of water in the kidneys

causes vasoconstriction and PVR to increase blood pressure

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18
Q

Perioperative causes of ADH release include:

A 
hemorrhage
positive pressure ventilation
upright position
nausea
medications
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19
Q

Renin is

A

enzyme secreted by the kidneys that hydrolyzes angiotensin to angiotensin 1

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20
Q

Where is renin released?

A

juxtaglomerular cells located near the afferent arterioles

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21
Q

What is renin released in response to?

A

a decrease in arterial blood pressure
a decreased in sodium load delivered to the distal tubules
SNS beta 1 receptors

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22
Q

Angiotension 1 is converted to angiotension 2 where?

A

the lungs

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23
Q

Angiotensin 2 is

A

a potent vasoconstrictor and stimulates the hypothalamus to secrete ADH

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24
Q

Aldosterone is a

A

mineralocorticoid hormone release from the adrenal gland

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25
Q

What is the plasma half-life of aldosterone?

A

20 minutes

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26
Q

What does aldosterone do?

A

stimulates epithelial cells in the distal tubule and collecting ducts to reabsorb sodium and water
exchanges potassium to maintain electroneutrality

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27
Q

What does aldosterone the opposite of?

A

atrial natriuretic hormone function

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28
Q

Acute kidney injury is defined as

A

sudden inability of the kidneys to vary urine volume and content appropriately

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29
Q

Causes of AKI

A

pre-renal
intrinsic renal
post renal

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30
Q

Characteristics of AKI

A

develops rapidly but may resolve

has a 50% mortality rate

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31
Q

Spiralactone is what diuretic?

A

potassium sparing diuretic that blocks aldosterone receptors

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32
Q

Pre-renal is caused by

A

hemodynamic or endocrine factors that impair perfusion
hypoperfusion or hypovolemia
activates mechanism to conserve salt and water
can progress to permanent parenchymal damage

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33
Q

Examples of hypoperfusion or hypovolemia (pre-renal)

A 
skin loss
fluid loss
hemorrhage
sequestration
vascular occlusion (thrombosis, aortic or renal artery clamping)
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34
Q

Renal or Acute Tubular Necrosis (ATN)

A

tissue damage from prolonged ischemia or nephrotic injury, glomerulonephritis

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35
Q

Patients with parenchymal disease will have trouble

A

concentrating urine

high urine sodium and low osmolality

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36
Q

Post-renal d/t

A

obstruction (calculi, blood clots, neoplasm)
surgical ligation
edema

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37
Q

Oliguric

A

<0.5ml/kg/hr

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38
Q

Polyuric

A

> 2.5L/day of non-concentrated urine

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39
Q

Risk factors for AKI/AKF

A 
renal reserve decreases with age
pre-existing renal dysfunction
cardiac bypass, aortic aneurysms (supra-renal aortic clamping), ventricular dysfunctions
sepsis
use of nephrotoxic agents
diabetes, HTN
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40
Q

Contrast Induced Nephropathy

A

results from administration of iodinated contrast media

transient and reversible form of acute renal failure

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41
Q

What is the treatment of CIN?

A

mainly supportive, consisting of careful fluid and electrolyte management although dialysis may be required in some cases

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42
Q

What is the suggested pathology of CIN?

A

direct toxicity of CM which could be related to harmful effects of free radicals and oxidative stress
while in renal tubules, excreted CM generates osmotic force causing marked increase in sodium and water excretion
diuresis will increase intratubular pressure which will reduce the GFR contributing to the pathogenesis of acute renal failure

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43
Q

Treatment of CIN

A

only supportive
prevention key
risk vs benefit should be considered

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44
Q

Oliguria is a sign of

A

inadequate systemic perfusion

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45
Q

What monitors can assess fluid status intraoperatively

A 
urinary catheter
TEE
CVP
blood pressure
SVV
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46
Q

How do you treat oliguria?

A

assume prerenal oliguria is related to fluid until proved otherwise
selective dopamine DA1 receptor agonist can cause renal arteriolar vasodilation
-fenoldopam, low dose dopamine

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47
Q

What do you not give in the setting in intravascular hypovolemia?

A

diuretics
furosemide
mannitol

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48
Q

What population has a 1.5 greater risk of developing kidney failure?

A

hispanic americans

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49
Q

ESRD rates are how many time higher among African americans in comparison to whites?

A

4 fold

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50
Q

How many more times are native americans likely to be diagnosed with kidney failure?

A

1.8

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51
Q

What is the leading cause of kidney failure among american indians

A

diabetes

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52
Q

What is most prevalent among african american and major cause of ESRD in this population?

A

hypertension

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53
Q

what increased the risk of developing kidney disease and limit access to preventive measure and treatment in communities with socioeconomic and cultural differences?

A 
language barriers
education and literacy levels
low income
unemployment
lack of adequate health insurance 
certain culture-specific health belieds and practices
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54
Q

Chronic renal failure is

A

slow progressive irreversible
decreased functioning nephrons
decreased RBF
decreased GFR, tubular function, and reabsorptive capacity

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55
Q

Common causes of chronic renal failure

A 
glomerulonephritis
pyelonephritis
diabetes
vascular or hypertensive insults
congenital defects
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56
Q

Stages of Chronic renal failure

A

decreased renal reserve
renal insufficiency
end stage renal failure or uremia

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57
Q

Decreased renal reserve is asymptommatic until

A

<40% of normal nephron remain

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58
Q

Define renal insufficiency

A

10-40% of functioning nephrons remain

compensated, little renal reserve

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59
Q

Define end stage renal failure or uremia

A

> 95% of nephrons are nonfunctioning
GFR is <5-10% of normal
Severely compromised electrolyte, hematologic, and acid-base balances
Dialysis dependent

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60
Q

In ESRF, what is eventually lethal?

A

uremia

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61
Q

What are the six manifestations of chronic renal failure?

A 
hypervolemia
acidemia
hyperkalemia
cardiorespiratory dysfunction
anemia
bleeding disturbances
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62
Q

What are the three treatments of chronic kidney failure?

A

hemodialysis
peritoneal dialysis
kidney transplant

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63
Q

What are the four components of a urinalysis?

A

specific gravity
urine osmolality
proteinuria
urinary pH

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64
Q

Define specific gravity

A

measurement of solutes in the urine, indicates kidneys ability to excrete concentrated urine. It reflect tubular function

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65
Q

CHF, Liver Failure can lead to

A

hypovolemia, decreased CO and decreased effective circulating volume

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66
Q

NSAIDs, ACE inhibitors and cyclosporine can lead to

A

impaired kidney autoregulation

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67
Q

hypovolemia, decreased CO and decreased effective circulating volume and impaired kidney autoregulation can cause

A

pre-renal AKI

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68
Q

Two causes of Post- renal AKI are

A

bilateral uretotrophic obstruction

bladder outlet obstruction

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69
Q

ischemia, sepsis and nephrotoxins can lead to

A

acute glomerulophritis, tubular damage

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70
Q

Vascularitis, TTP/HUS and Malignant hypertension can lead to

A

vascular damage

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71
Q

vascular damage and acute glomerulophritis, tubular damage can lead to

A

Intrinsic renal AKI

72
Q

GFR criteria and UOP criteria for renal failure risk

A

increased Cr x1.5 or GFR decrease <25%

UO <0.5ml/kg/hr x 6h

73
Q

GFR criteria and UOP criteria for Renal Injury

A

Increased creatinine x2 or GFR decrease >50%

UO <0.5ml/kg/hr x 12 hrs

74
Q

GFR criteria and UOP criteria for Renal failure

A

increased creatinine x3 or GFR decrease > 75% or creatinine >4mg/ 100ml (acute rise of >0.5mg per 100ml/dl)
OU <0.3ml/kg/hr x 24 hour or anuria x 12 hr

75
Q

What does selective dopamine DA1 receptor agonist do?

A

causes renal arteriolar vasodilation
Fenoldopam
Low dose dopamine

76
Q

3-10mcg of dopamine effects

A

increases contractility,
minimal change in HR and SVR
increase Renal BF
increase splanchnic BF

77
Q

> 10 mcg dopamine effects

A

increase HR, vasoconstriction, decrease/increase renal BF, increase decrease splanchnic BF

78
Q

> 10 mcg dopamine effects

A

increase HR, vasoconstriction, decrease/increase renal BF, increase decrease splanchnic BF

79
Q

Three causes of pre-renal failure

A

absolute decrease in ECF volume
decreased RBF
altered intra-renal hemodynamics

80
Q

Examples of absolute decrease in ECF volume for pre-renal failure

A

GI losses

hemorrhages

81
Q

Examples of decreased RBF for pre-renal failure

A

heart failure

renal artery stenosis

82
Q

Examples of altered intra-renal hemodynamics for pre-renal failure

A 
Drug induced- NSAIDs/COX 2 inhibitors
calcineurin inhibitors
ACE inhibitors
Angiotensin 2 receptor blockers
sepsis
hypercalcemia
cirrhosis, Hepatorenal syndrome
abdominal compartment syndrome
83
Q

Two causes of intra-renal failure

A

tubulo-interstitial disorders

glomerular disorders

84
Q

Types of tubulo-intestitial disorders for intra-renal failure

A 
tubular injury (ischemic, nephrotic)
Interstitial nephritis (allergic type or NSAID type)
85
Q

Types of glomerular disorders for intra-renal failure

A

glomerulonephritis
thrombotic microanglopathies
atheroembolic disease

86
Q

Two causes of post-renal failure

A

anatomic obstruction

tubular obstruction

87
Q

Types of anatomic obstruction for post-renal failure

A 
bladder outlet (prostate, pelvic tumor)
ureteral (tumor, stones, strictures)
88
Q

Types of tubular obstructution causing post-renal failure

A

crystals (Calcium oxalate
Drugs: indinavir, methotraxate
proteins (myeloma cast neuropathy)

89
Q

Define urine osmolality

A

the number of moles per solute per kilogram of solvent
more specific than specific gravity
ability to excrete concentrated urine indicates good tubular function

90
Q

Define proteinuria

A

when >150mg is excreted per day
when >750mg (3+ or 4+) is indicative of severe glomerular famage
failure of renal tubules to reabsorb protein

91
Q

Define urinary pH

A

inability to excrete an an acid urine in the presence of acidosis is indicative of renal insufficiency

92
Q

Glucose is freely filtered where?

A

the glomerulus

93
Q

Where is glucose reabsorbed?

A

proximal tubule

94
Q

Glycosuria is a sign

A

that the ability of the renal tubules to reabsorb glucose has been exceeded by an abnormally heavy glucose load
usual indicative of diabetes

95
Q

What are the 4 laboratory tests for renal function

A

BUN
serum creatinine
Creatinine clearance
glomerular filtration rate

96
Q

Define BUN

A

blood urea nitrogen
not a direct measure of renal function
influenced by exercise, steroids, and tissue breakdown

97
Q

When is BUN elevated?

A

when kidney disease is reduced to about 75%

98
Q

Define serum creatinine

A

muscle tissue turnover and dietary intake of protein

99
Q

How is creatinine treated at the glomerulus?

A

freely filtered and neither reabsorbed or secreted

100
Q

What is a good measure of GFR?

A

creatinine clearance

101
Q

What is the best measure of glomerular function?

A

glomerular filtration rate

102
Q

What is a normal GFR?

A

125ml/min

103
Q

What is an symptomatic GFR?

A

<30-50% of normal GFR

104
Q

What can be seen in an electrocardiogram in patients with renal disease?

A

peaked T waves

small or indiscernible P waves

105
Q

What clinical situations contribute to increased K in renal failure patients?

A 
LR
Succinylcholine
acidosis, electrolytes
missed dialysis
Vomiting
diarrhea
rhabomylasis
106
Q

During blood storage what consistently leaks from cells?

A

potassium

107
Q

How long are RBCs stored in blood bank?

A

42 days

108
Q

How can potassium overload from transfusion be avoided?

A

using blood less then 5 days old

washing any unit of blood immediately before infusion to remove extracellular potassium

109
Q

What does US describe in renal disease?

A

kidney size, hydronephrosis, vasculature, obstructions and masses

110
Q

What does CT describe in renal disease?

A

detects stones of all kinds, masses may be evaluated using contrast

111
Q

What does MRI describe in renal disease?

A

detailed tissue characterization, nice alternative to a contrast CT, reduced radiation exposure

112
Q

What is gadolinium?

A

paramagnetic intravenous contrast agent

commonly used in MRA

113
Q

What effects does GA have on renal function?

A

Pulse pressure variation and CO decrease

causing depression of renal BF, GFR, urinary flow and electrolyte secretion

114
Q

What effect does regional anesthesia have on renal function?

A

parallels with degree of SNS blockade
decreased venous return
decrease in blood pressure

115
Q

What are the peri-operative indirect effects of anesthesia on renal function?

A

circulatory and endocrine, SNS and patient positioning

116
Q

What are the direct peri-operative effects of anesthesia on renal function?

A

medications that target renal cellular function

117
Q

What is the effect of surgery on renal function?

A

stress and catecholamine release
fluid shifts
secretion of vasopressin and angiotensin

118
Q

What are the three opioids effected by renal function?

A

morphine, meperidine, fentanyl

119
Q

Why is morphine important in renal function?

A

active metabolite that depend on renal clearance mechanisms for elimination
principally metabolized by conjugation in the liver, and water soluble glucuronides (morphine 3 and morphine-6 glucoronide) are excreted via the kidney

120
Q

Why is meperidine important to note with renal function?

A

active metabolite, normeperidine, depended on renal excretion
accumulation can lead to seizures and CNS toxicity

121
Q

Why is fentanyl important to note with renal function?

A

not grossly altered by renal failure, but a decrease in plasma protein binding may result in higher free fractions
Ie decrease dose

122
Q

Is ketamine dosing increased or decreased in CKD? Why?

A

not needed despite being metabolized in liver into active metabolite then metabolite being excreted in kidney

123
Q

Name two gabapentinoids

A

gabapentin (neurtonin) and pregabalin (lyrica)

124
Q

How are gabapentinoids effected in CKD?

A

liberal administration can increase risk of over sedation and coma
Agents do not undergo hepatic metabolism and are excreted solely by kidneys
reduction of 50% of the dose for each 50% decline in GFR or CCr and increasing time interval between dose recommended

125
Q

What physiological renal responses occur with VA?

A

decrease in BP and kidneys increase renal vascular resistance causing decrease in renal blood flow

126
Q

Isoflurane and renal physiological response

A

decrease BP in dose dependent fashion

127
Q

Desflurane and renal physiological response

A

with increase HR, may maintain a greater degree of cardiac output and therefore renal perfusion

128
Q

Sevoflurane and renal physiological response

A

free fluoride ion metabolite

compound A

129
Q

When can compound A occur?

A

CO2 absorbents containing soda lime (KOH, NaOH, h20, CaOH2) degrade sevo resulting in production of vinyl ether

130
Q

Risk of compound A exposure is dependent on (3)

A

duration of exposure
fresh gas flow rate
concentration of sevoflurane

131
Q

Succinylcholine causes a rapid, transient increase in serum potassium by

A

0.5mEq/L

132
Q

In patients with renal failure, succinylcholine can

A

be exaggerated to >0.5mEq/L

133
Q

When is succinylcholine okay (with caution) to use in renal patient?

A

dialysis within 24 hours and normal serum K+

134
Q

Non-depolarizing muscle relaxants and renal failure

A

the duration of action may be prolonged with renal failure

135
Q

what two NDMRs are not effected by renal failure

A

cisatracurium and atracurium

136
Q

How is sugammadex excreted?

A

the resultant sugammadex neuromuscular blocker complex by the kidney

137
Q

What is an intermediate in the metabolism of sodium nitroprusside?

A

cyanide

138
Q

What is the final metabolic product of sodium nitroprusside?

A

thiocyanate

139
Q

Is the half life of thiocyanate prolonged in renal failure?

A

yes, normal 4 days but longer in CKF

140
Q

Describe albumin role in kidney disease

A

may be protective by maintaining renal perfusion, binding of endogenous toxins and nephrotic drugs and preventing oxidative damage

141
Q

What fluids can be associated with acute kidney injury and should be avoided?

A

hetastarch/ dextran

142
Q

how hetastarch cause AKI?

A

breakdown of the synthetic carbohydrates to degradation products that cause direct tubular injury and plugging of tubules

143
Q

What drugs can impair renal doses to dopamine?

A

anti-dopaminergics

metoclopramide, phenothiazines, droperiodol

144
Q

Dopamine and fenoldopam

A

dilate afferent and efferent arterioles and increase renal perfusion
selective D1 agonist

145
Q

What are the four renal pathophysiologies that require surgery?

A

renal cell carcinoma
renal dysplasia
polycystic kidney disease
wilm’s tumor

146
Q

what is the most common renal malignancy?

A

renal cell carcinoma

147
Q

Where does renal cell carcinoma originate?

A

proximal tubules

148
Q

What is the cure to renal cell carcinoma?

A

surgical resection

refractory to chemo and radiation

149
Q

What is the triad of renal cell carcinoma?

A

hematuria
flank pain
renal mass

150
Q

When may CBP be needed for renal cell carcinoma?

A

when the tumor extens into the renal vein and the IVC and right atrium

151
Q

What is renal dysplasia?

A

malformation of the tubules during fetal development

consists of irregular cysts of various sizes

152
Q

how is renal dysplasia diagnosed?

A

in utero by US

153
Q

Ureteropelvic junction and vesicoureteral reflux is also seen with

A

renal dysplasia

154
Q

What does renal dysplasia lead to?

A

CKD, dialysis, transplant

155
Q

Polycystic kidney disease is

A

an inherited massive enlargement of kidneys with compromised renal funciton
cyst can also occur on other organs (liver, pancreas, spleen)
non-functioning fluid filled cysts that range in size from small to mass effect producing size

156
Q

How is polycystic kidney disease painful?

A

due to distention of cysts and stretching of fascia

157
Q

What exacerbates PKD pain?

A

hemorrhage, rupture or infection

158
Q

How does PKD progress into adulthood?

A

bilateral disease

159
Q

Complications of PKD

A

HTN due to activation of RAAS
cyst infection
bleeding
decline in renal function

160
Q

Treatment of PKD

A

symptom management
dialysis
transplant

161
Q

How does wilm’s tumor present?

A

unilaterally and painless, palpable mass

162
Q

what is wilm’s tumor associated with?

A

congenital/genetic malformations

Beckwith-wiedermann and WAGR

163
Q

What is the most common malignant tumor in children?

A

wilm’s tumor

1/3 occur in age under 1

164
Q

Where does wilm’s tumor metastasize?

A

lungs

165
Q

treatment of wilm’s tumor includes?

A

resection and possible chemotherapy

capacity for rapid growth

166
Q

Name the 5 stages of wilm’s tumor

A

stage 1: limited to kidney and completely excised
stage 2: tumor extends beyond the kidney but is completely excised
stage 3: inoperable primary tumor of lymph node metastasis
Stage 4: lymph node metasases outside the abdominal pelvic region
Stage 5: bilateral renal involvement

167
Q

Total nephrectomy

A

renal artery and vein are ligated and then it involves removal of the kidney, the ipslateral adrenal gland, perinephric fat, and the surrounding tissue

168
Q

partial nephrectomy

A

nephron sparing
considered with patients with solitary functional kidney, small leisons (< 4cm) or bilateral tumors, or for patients with increased risk because of other diseases such as diabetes or hypertension

169
Q

Anesthetic requirements for nephrectomy

A 
standard risk assessment
identify smoking and age risk factors
note any pre-existing renal dysfunction
many are anemic (CBC and TC)
K (BMP)
regional anesthesia include blockade of nerve roots T8-L3
ERAS
Opioid sparing
170
Q

PTH increased Ca++ reabsorption exchanges

A

phosphate

171
Q

Erythropoietin is

A

released by kidney in response to anemia, hypoxia

172
Q

aldosterone is secreated from

A

adrenal cortex and causes reabsorption of Na

173
Q

ADh/Vasopressin constricts

A

efferent arteriole and reabsorbs water

174
Q

ANP

A

atrial distension (fluid overload) stimulates excretion of sodium and water

175
Q

Dopamine is what receptor in renal vasculature and excretes?

A

Da1 receptor

sodium excretion

N935 Advanced Pathophysiology (9 decks)

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