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N935 Pathophysiology > Renal Pathophysiology > Flashcards

Renal Pathophysiology Flashcards

1
Q

kidneys receive how much total cardiac output

A

15-25%

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2
Q

how much of the blood directed towards the kidneys is directed towards the renal cortex

A

95%

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3
Q

how much of the blood directed towards the kidneys is directed towards the medulla

A

~5%

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4
Q

how many L/min of blood flows through the renal arteries

A

1-2.5L/min

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5
Q

what part of the kidney is most vulnerable to ischemic insults

A

renal medullary papillae

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6
Q

what is the mmHg range in which kidneys auto regulate their mean arterial pressures

A

60-160mmHg

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7
Q

is auto regulation intact in a denervated kidney

A

yes

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8
Q

what regulates autoregulation of the kidneys

A

intrinsic mechanisms of the kidney itself. they auto regulate via vasodilation and vasoconstriction of renal afferent arterioles

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9
Q

what separates the afferent arterioles from the efferent arterioles

A

glomerulus

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10
Q

how is hydrostatic pressure created in the kidney

A

resistance from efferent arterioles, which provides force for ultrafiltration

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11
Q

podocytes

A

endothelial cells that line the capillaries in the kidney

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12
Q

glomerular filtration rate

A

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

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13
Q

how does SNS activation affect renal blood flow

A

reduces renal blood flow

stimulated via adrenal medulla to release catecholamines of if BP decreases SNS will also stimulate RAAS

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14
Q

how does surgical stimulation affect vascular resistance

A

it increases vascular resistance

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15
Q

when is ADH released

A

in response to decreased stretch receptors in the atrial and arterial wall
released in response to increased osmolality of the plasma (monitored by hypothalamus) aka dehydration

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16
Q

where is ADH synthesized and released

A

hypothalamus, released from posterior ptuitary

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17
Q

half life of ADH

A

16-24h

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18
Q

2 primary functions of ADH

A

increases reabsorption of sodium and water in the kidneys

causes vasoconstriction and PVR to increase BP

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19
Q

perioperative causes of ADH (5)

A 
hemorrhage
PPV
upright position of position changes
nausea
medications
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20
Q

role of renin

A

secreted by kidneys, hydrolyzes angiotensin to angiotensin 1

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21
Q

what is released from the juxtaglomerular cells

A

renin

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22
Q

what is renin released at the juxtaglomerular cells in response to (3)

A

decreased arterial BP
decrease in sodium load delivered to distal tubules
SNS (beta 1 receptors)

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23
Q

angiotensin I and II conversion

A

angiotensin I is converted in the lungs by angiotensin converting enzyme (ACE) into angiotensin II

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24
Q

role of angiotensin II

A

potent vasoconstrictor, stimulates hypothalamus to secrete ADH

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25
Q

aldosterone released from

A

minteralcorticoid hormone released from adrenal gland

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26
Q

plasma half life of aldosterone

A

20 minutes

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27
Q

role of aldosterone

A

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

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28
Q

what is the complete opposite of aldosterone function

A

atrial natriuretic peptide (ANP)

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29
Q

spironolactone works by

A

potassium sparing diuretic that blocks aldosterone receptors

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30
Q

causes of AKI can be categorized as (3)

A

prerenal, infrarenal, postrenal

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31
Q

definition of pre renal AKI

A

hemodynamic or endocrine factors that impair perfusion. can progress to permanent parenchymal damage

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32
Q

causes of pre renal AKI (7)

A

hypo perfusion or hypovolemia
skin loss (burns)
absolute decrease in ECF volume (fluid loss, hemorrhage)
sequestration
vascular occlusion (thrombosis, aortic or renal artery clamping)
decreased renal blood flow (heart failure, renal artery stenosis)
altered hemodynamics (abdominal compartment syndrome, hepatorenal, hypercalcemia, sepsis, drugs)

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33
Q

pre-renal AKI usual pathology to correct itself

A

RAAS, ADH, low urine sodium with high osmolality

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34
Q

reasons for renal or acute tubular necrosis (ATN)

A

tissue damage from prolonged ischemia, nephrotic injury (antibiotics, chemotherapeutics, contrast dye), glomerulonephritis

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35
Q

what do you expect with a urinalysis from an ATN patient

A

patients with parenchymal disease will have trouble concentrating urine
you will see high urine sodium and low osmolality

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36
Q

nephrotoxic drugs include

A

aminoglycosides!!!!!! (gentamicin, tobramycin)
chemotherapeutic agents
NSAIDS
radiocontrast dye

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37
Q

post renal AKI causes

A

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

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38
Q

oliguria

A
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39
Q

polyuria

A

> 2.5L/day of non concentrated urine

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40
Q

renal failure risk based on creatinine, UOP, GFR

A

creatinine increase x1.5 OR
GFR decrease >25%
UO

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41
Q

renal injury based on creatinine, UOP, GFR

A

increased creatinine x2 OR
GFR decrease >50%
UOP

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42
Q

renal failure based on creatinine, UOP, GFR

A

increased creatinine x3 OR
GFR decrease >75% OR
creating >4mg/100mL
UOP

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43
Q

risk factors for acute renal failure/injury

A 
renal reserve decreasing with age
preexisting renal dysfunction
certain surgical procedures
sepsis
use of nephrotoxic agents
diabetes, HTN
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44
Q

risk factors for acute renal failure/injury: how much does renal reserve decrease with age

A

for each year after age 50, creatinine clearance decreases by 1.5mL’s and renal plasma flow by 8mL

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45
Q

risk factors for acute renal failure/injury: certain surgical procedures include

A 
cardiac bypass >2h
aortic aneurysms (supra renal aortic clamping)
ventricular dysfunctions
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46
Q

risk factors for acute renal failure/injury: sepsis includes

A 
hypovolemia
hemolysis
DIC
infections
acidosis
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47
Q

2 ways to prevent renal insult

A

hydration

BP maintenance

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48
Q

contrast induced nephropathy (CIN) result from

A

results from administration iodinated contrast media. transient and reversible form of acute renal failure
(iodinated=worst for kidneys)

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49
Q

contrast induced nephropathy (CIN) treatment

A

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

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50
Q

what are some risk factors that place a patient at increased risk for CIN

A

preexisting AKI
HTN
volume status
hepatorenal syndrome

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51
Q

CIN pathophysiology

A

worsened by hypoxia and hypoperfuson
direct toxicity of contrast media (CM) which could be related to harmful effects of free radicals and oxidative stress
in the renal tubules, excreted CM generates osmotic force causing marked increase in sodium and water excretion
this diuresis will increase intra tubular pressure, which will reduce GFR, contributing to pathogenesis of renal failure.

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52
Q

CIN and free radicals

A

it is thought that activation of cytokine induced inflammatory mediators by reactive free radicals is the responsible mechanism. conversely, the inhibition or reduction of free radicals formation might reduce CIN by alkalinizing tubular cells

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53
Q

CIN tx

A

only supportive, prevention is important

benefit for CM based diagnostic studies or interventional procedures should always be weighted against the risk of CIN

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54
Q

oliguria in the OR

A

often a sign of inadequate systemic perfusion. rapid recognition and tx can help prevent renal insult intra operatively

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55
Q

monitors to assess fluid status intra operatively

A 
urinary catheter
TEE
CVP
BP
SVV
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56
Q

what is the differential diagnosis for oliguria in the OR

A

pump problem versus volume status problem versus vasodilation problem

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57
Q

SVV >10% =

A

volume bolus indication (7mL/kg)

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58
Q

SVV <10%, CI <2.5L/min

A

catecholamines (epi until CI >2.5L/min)

59
Q

SVV >10%, CI >2.5L/min, MAP <60mmHg

A

vasopressor (norepinephrine until MAP >60)

60
Q

oliguria treatment

A

assume prerenal oliguria is related to fluid until proven otherwise

  • diuretics to consider are furosemide and mannitol, but do not consider these in the setting of hypovolemia
  • selective dopa agonist cases renal arteriolar vasodilation (fenoldapam, low dose dopa)
61
Q

examples of intra renal AKI reasons

A 
tubular injury (ischemia or nephrotoxicity)
interstitial nephritis (allergy or NSAID type)
glomerular DO's (glomerulonephritis, thrombotic micorangiopathies, atheroembolic disease)
62
Q

examples of post renal AKI reasons

A 
anastomotic obstruction of bladder outlet, ureter)
tubular obstruction (crystals, drug induced, proteins)
63
Q

leading causes of CKD

A

diabetes and HTN

64
Q

hispanic americans are at how much greater risk for developing kidney failure

A

1.5x

65
Q

how much higher are ESRD rates in african americans

A

4x

66
Q

native americans are how much more likely to be diagnosed with kidney failure?

A

1.8x

67
Q

chronic renal failure overview

A

slow, progressive, irreversible
decreased functioning nephrons
decreased renal blood flow
decreased GFR, tubular function, reabsorptive capacity

68
Q

common causes of chronic renal failure (5)

A

glomerulonephritis (inflammation of glomerulus)
pyelonephritis (kidney inflammation, usually UTI r/t E.coli)
DM
vascular or hypertensive insults
congenital defects

69
Q

chronic renal failure stages (3)

A

decreased renal reserve ->
renal insufficiency ->
end stage renal failure or uremia

70
Q

chronic renal failure stage 1: decreased renal reserve

A

asymptomatic until <40% of functioning nephrons remains

71
Q

chronic renal failure stage 2: renal insufficiency

A

10-40% of functioning nephrons remains

compensated, little renal reserve

72
Q

chronic renal failure stage 3: ESRF or uremia

A

> 95% of nephrons are non functioning
GFR is 5-10% of normal
severely compromised electrolyte, hematologic, and acid base balances
uremia (urine in blood) is eventually lethal
dialysis dependent

73
Q

chronic renal failure manifestations (6)

A 
hypervolemia
acidemia
hyperkalemia
cardiorespiratory dysfunction
anemia (EPO)
bleeding disturbances
74
Q

chronic renal failure treatment (3)

A

HD, PD, transplant

75
Q

SG reflects

A

tubular function. ability to concentrate urine

76
Q

glucose filtration and reabsorption in kidneys

A

freely filtered at glomerulus, reabsorbed in proximal tubule

77
Q

glycosuria

A

signifies ability of renal tubules to reabsorb glucose has been exceeded by abnormally heavy glucose lead and is usually indicative of DM

78
Q

lab test for renal function: blood urea nitrogen (BUN)

A

not a direct renal function. influenced by exercise, bleeding, steroids, and tissue breakdown. elevates in kidney disease once GFR is reduced to ~75%

79
Q

lab test for renal function: serum creatinine

A

muscle tissue turnover and dietary intake of protein. creatinine is freely filtered at glomerulus and is neither reabsorbed nor excreted

80
Q

lab test for renal function: GFR

A

best measure of glomerular function. normal is 125mL/min. asymptomatic until GFR decreases to <30-50% of normal

81
Q

conditions causing elevation of serum creatinine independent of GFR

A

ketoacidosis
cephalothin, cefoxitin
flu cytosine
other drugs including aspirin, cimetidine, probenecid, trimethoprim

82
Q

conditions causing decrease of serum creatinine independent of GFR

A

physiologic decrease in muscle mass, pathologic decrease in muscle mass, decreased hepatic creatine synthesis and cachexia

83
Q

when giving PRBC’s to ESRD, consider the following to reduce incidence of hyperkalemia

A

select <5d old blood
wash any unit of blood immediately before transfusion to remove extracellular K
using filters helps
rate and volume of transfusion also plays a role

84
Q

imaging studies in renal disease: ultrasound

A

noninvasive, minimal patient prep, assess kidney size, hydronephrosis, vasculature, obstructions, masses

85
Q

imaging studies in renal disease: CT

A

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

86
Q

imaging studies in renal disease: MRI

A

detailed tissue characterization, nice alternative to a contrast CT, reduced radiation exposure (ex preggo)

87
Q

gadolinium

A

paramagnetic intravenous contrast agent commonly used in MRA images

88
Q

peri operative effects on renal function: GA

A

PPV and decreased CO depresses renal blood flow, GFR, urinary blood flow, and electrolyte sevretion

89
Q

peri operative effects on renal function: regional anesthesia

A

parallels with degree of SNS blockade, decreased VR, and decrease in blood pressure

90
Q

peri operative effects on renal function: indirect effects

A

circulatory, endocrine, SNS, patient positioning

91
Q

peri operative effects on renal function: direct effects

A

medications that target renal cellular function

92
Q

peri operative effects on renal function: surgery

A

stress and catecholamine release, fluid shifts, secretion of vasopressin and angiotensin

93
Q

morphine

A

active metabolites that depend on renal clearance mechanisms for elimination. principally metabolized by conjugation in the liver, and the water soluble glucoronides are excreted by kidney. morphine 6 glucoronide is active
dont give this drug in ARF

94
Q

meperidine

A

active metabolite normeperidine depends on renal excretion. accumulation can lead to CNS toxicity and seizures

95
Q

fentanyl

A

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

96
Q

hydromorphone dosage trend and CKD

A

decrease dosage as ESRD gets worse

97
Q

CKD and ketamine

A

8% of administered ketamine is metabolized by liver forming norketamine (non active). norketamine is then hydroxylated into a water soluble metabolite excreted by the kidney. most clinicians believe that dose modification for ketamine is not required.

98
Q

gabapentinoids (gabapentin, pregabalin) and CKD

A

do not undergo hepatic metabolism and are excreted solely by the kidney. a reduction of 50% of dose for each 50% decline in GFR or creatinine clearance and increasing the time interval between each dose is advised.

99
Q

inhalation agents and renal: isoflurane

A

decreases BP (dose dependent)

100
Q

inhalation agents and renal: desflurane

A

with increased HR, may maintain greater degree of CO and therefore renal perfusion

101
Q

inhalation agents and renal: sevoflurane

A

free fluoride ion metabolite. was more pronounced and only proven with methoxyflurane (and >5 mac hours) and clear evidence has not been established with sevoflurane

102
Q

compound A

A

CO2 absorbents containing some line degrade sevoflurane resulting in production of vinyl ether compound called compound A.

103
Q

risk for compound A is dependent on (3)

A

duration of exposure
FGF rate
concentration of sevo (mac hours)

104
Q

AMSORB

A

replaces soda lime
is non caustic and can be disposed of in domestic waste
no production of compound A even when desiccated and low flows with sevo are safe

105
Q

propofol

A

dose not adversely effect renal tubular function
may be an extra hepatic site of propofol disposition (along with liver and small intestine glucoronidation)
prolonged infusions may result in green urine due to presence of phenolic metabolites (discoloration does not affect renal function)

106
Q

propofol infusion syndrome can result in renal failure secondary to

A

rhabdomyolysis
myoglobinuria
hypotension
metabolic acidosis

107
Q

succinylcholine

A

can be used carefully. metabolism is catalyzed by pseudocholinesterase to yield nontoxic succinic acid and choline. .5mEq/L transient increase in K can be exaggerated in patient with renal failure.
okay if patient has receive HD within 24h and has normal K

108
Q

metabolic precursor of succinc acid and choline and where its excreted

A

succinylmonocholine is excreted via the kidneys

109
Q

DOA of muscle relaxants my be _______ in patients with renal failure

A

prolonged

110
Q

sugammadex

A

cyclodextrin molecule that inactivates aminosteroidal NMB’s, resultant sugammadex NMB complex is excreted by the kidney. in patient with severe renal impairment, cyclodextrin complexes can accumulate. insufficient data of what long term exposure to the complexes means

111
Q

sodium nitroprusside

A

cyanide is an intermediate in the metabolism of sodium nitroprusside, with thiocyanate being the final metabolic end product

112
Q

half life of thiocyanate

A

normally >4d, and is prolonged in patients with renal failure

113
Q

s/sx of thiocyanate levels >10mg/100mL

A

hypoxia, nausea, tinnitus, muscle spasm, disorientation, and psychosis

114
Q

thiocyanate toxicity associated with

A

long term infusions (usually >6d)

115
Q

albumin

A

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

116
Q

hetastarch/dextran

A

associated with AKI secondary to breakdown of synthetic carbohydrates to degradation products that cause direct tubular injury and plugging of tubules. worsened by decreased renal perfusion

117
Q

dopaminergics

A

dopamine and fenoldapam (selective D1 agonist) dilate afferent and efferent arterioles and increase renal perfusion

118
Q

anti dopaminergics

A

(metoclopramide, phenothiazines, droperidol) may impair renal response to dopamine

119
Q

renal pathophysiology requiring surgery (4)

A

renal cell carcinoma
renal dysplasia
PKD (polycystic kidney disease)
wilms tumor

120
Q

renal cell carcinoma

A

most common renal malignancy
originates in lining of proximal tubular
refractory to chemo or radiation
surgical resection is often curative

121
Q

renal cell carcinoma triad

A

hematuria, flank pain, renal mass.

122
Q

renal cell carcinoma extensions would be found

A

5-10%, the tumor extends into renal vein and IVC and RA. may then require CPB.

123
Q

renal dysplasia

A

malformation of tubules during fetal development (modern family girl)
kidney consists of irregular cysts of varying sizes
dx often made in utero by US
may also have ureteropelvic function obstruction and vesicoureteral reflux
linked to genetic mutation and illicit drug use by mother
bilateral is incompatible with survival
about 90% of patients will have contralateral hypertrophy by adulthood for compensation

124
Q

renal dysplasia can lead to (3)

A

CKD, HD, transplant

125
Q

polycystic kidney disease (PKD)

A

inherited (dominant or recessive), massive engagement of kidneys with compromised renal function.
cysts can also occur on other organs (liver, pancreas, spleen)
painful due to distention of cysts and stretching of fascia.
hemorrhage, rupture, or infection exacerbate this pain
non functioning fluid filled cysts that range in size from microscopic to mass effect producing size
most cases progress to bilateral disease by adulthood

126
Q

complications of PKD (4)

A

HTN d/t activation of RAAS
cyst infections
bleeding
decline in renal function

127
Q

PDK tx

A

sx management
HD
transplant

128
Q

wilms tumor (nephroblastoma)

A

often presents unilaterally and a painless, palpable abdominal mass.
can be associated with congenital/genetic malformations
most common malignant renal tumor in children
requires resection and possible chemo
capacity for rapid growth

129
Q

where would wilms tumor likely metastasize to

A

lungs

130
Q

wilms tumor tx

A

resection and possibly chemo

131
Q

stages of wilms tumor, stage 1:

A

43% of classes, limited to kidney and is completely excised

132
Q

stages of wilms tumor, stage 2:

A

23% of vases, tumor extends beyond the kidney but is completely excised

133
Q

stages of wilms tumor, stage 3:

A

20% of vases, inoperable primary tumor or lymph node metastasis

134
Q

stages of wilms tumor, stage 4:

A

lymph node metastases outside of abdominopelvic region

135
Q

stages of wilms tumor, stage 5:

A

bilateral renal involvement

136
Q

total nephrectomy

A

renal artery and vein are ligated and then it involves removal of the kidney, ipsilateral adrenal gland, peirnephric fat, and surrounding fascia. other kidney needs to be functional

137
Q

partial nephrectomy

A

nephron sparing surgery, considered for patients with solitary functional kidney, small lesions (<4cm), or bilateral tumors, or for patents with increased risk because of other diseases, such as DM or HTN

138
Q

how are nephrectomies performed

A

open, lap, and/or robotic

139
Q

nephrectomy pre surgery considerations (4)

A

flank mass, HTN (on antihypertensives), US and CT, biopsy and dx

140
Q

nephrectomy anesthesia plan of care

A

premedicaiton
inhalation induction if pedes
BP control (hyper dynamic, volume and pressors plausible)
PIV x 2, aline, CVC placed by surgeon if used for chemo or by anesthesia for IV immunosuppression medication

141
Q

anesthesia considerations for nephrectomy

A 
standard risk assessment
ID smoking and age risk factors
note any preexisting renal dysfunction
many are anemic, get CBC and type/cross
BMP to assess K
regional anesthesia includes blockage of nerve roots T8-L3
ERRAS
opioid sparing
142
Q

PTH increased _______ in exhange for _________

A

Ca reabsorption in exchange for phosphate

143
Q

where is aldosterone secreted from

A

adrenal cortex, causes reabsorption of Na

N935 Pathophysiology (12 decks)

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