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N935 Advanced Pathophysiology II > Renal Pathophysiology > Flashcards

Renal Pathophysiology Flashcards

1
Q

how much cardiac output do the kidneys receive?

A

15-25%

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2
Q

how much blood goes to the renal cortex?

A

95%

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3
Q

how much blood goes to the renal medulla?

A

5%

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4
Q

blood flow through renal arteries

A

1-1.25 L/min

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5
Q

kidney autoregulation of blood flow

A
  • kidneys autoregulate their blood flow between 60-160 mmHg mean arterial pressures
  • intrinsic mechanism that causes vasodilation and vasoconstriction of the renal afferent arterioles regulates the autoregulation of renal blood flow
  • because it is intrinsic, autoregulation is intact even in denervated kidneys
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6
Q

glomerulus

A
  • separate afferent arterioles from efferent arterioles
  • the resistance in the efferent arterioles creates hydrostatic pressure within the glomerulus to provide force for ultrafiltration
  • capillaries are lined with endothelial cells (podocytes)
  • the rate at which blood is filtered through all the glomeruli (GFR) is a measure of overall kidney function
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7
Q

SNS activation + renal blood flow

A
  • reduction of renal blood flow
  • 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 RAAS
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8
Q

antidiuretic hormone

A
  • released in response to decreased stretch receptors in atrial and arterial wall
  • released in response to increased osmolality of the plasma (monitored by hypothalamus)
  • synthesized in hypothalamus and released from posterior pituitary
  • half life = 16-24 min
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9
Q

2 primary functions of ADH

A
  • increases reabsorption of sodium and water in the kidneys

- causes vasoconstriction and PVR to increase blood pressure

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10
Q

perioperative causes of ADH release

A
  • hemorrhage
  • positive pressure ventilation (decreased VR)
  • upright position
  • nausea
  • medications
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11
Q

renin

A
  • enzyme secreted by the kidneys that hydrolyzes angiotensinogen to angiotensin I
  • released from the JG cells located near afferent arterioles
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12
Q

what is renin released in response to?

A
  • a decreased arterial blood pressure
  • a decrease in sodium load delivered to the distal tubules
  • SNS (beta 1 receptors)
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13
Q

Angiotensin I

A

converted in the lungs by angiotensin-converting enzyme into angiotensin II

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14
Q

Angiotensin II

A

potent vasoconstrictor and stimulates the hypothalamus to secrete ADH

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15
Q

aldosterone

A
  • mineralocorticoid hormone released from adrenal gland
  • plasma half life = 20 minutes
  • stimulates epithelial cells in distal tubule and collecting ducts to reabsorb sodium and water (exchanges potassium to maintain electroneutrality)
  • complete opposite of atrial natriuretic hormone function
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16
Q

spironolactone

A

potassium sparing diuretic that blocks aldosterone receptors

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17
Q

acute renal failure

A
  • the sudden inability of the kidneys to vary urine volume and content appropriately
  • develops rapidly but may resolve
  • has a 50% mortality rate
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18
Q

pre-renal acute renal failure

A
  • hemodynamic or endocrine factors that impair perfusion
  • hypoperfusion or hypovolemia –> skin loss (burns), fluid loss, hemorrhage, sequestration, vascular occlusion (thrombosis or renal artery/aortic clamping)
  • will activate mechanism to conserve salt and water (RAAS, ADH)
  • can progress to parenchymal damage
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19
Q

pre renal failure labs

A
  • low urine sodium

- high urine osmolality

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20
Q

renal or acute tubular necrosis (intrarenal)

A
  • tissue damage - prolonged ischemia, nephrotic injury (abx, contrast, chemo), glomerulonephritis
  • patients with parenchymal disease will have trouble concentrating urine
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21
Q

intrarenal failure labs

A
  • high urine sodium

- low urine osmolality

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22
Q

post-renal acute renal failure

A
  • obstruction (calculi, blood clot, neoplasm)
  • surgical ligation
  • edema
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23
Q

oliguric

A

<0.5 mL/kg/hr

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24
Q

polyuric

A

> 2.5 L/day of non-concentrated urine

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25
Q

risk factors for acute renal failure/injury

A
  • age (renal reserve decreases with age)
  • preexisting renal dysfunction
  • certain surgical procedures (cardiac bypass >2 hours, aortic aneurysms with supra-renal clamping, ventricular dysfunctions)
  • sepsis (hypovolemia, hemolysis, DIC, infection, acidosis)
  • use of nephrotoxic agents
  • DM
  • HTN
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26
Q

contrast induced nephropathy (CIN)

A
  • 3rd most common cause of hospital acquired acute renal injury and represents
  • 12% of cases
  • results from administration of iodinated contrast media
  • transient and reversible
  • treatment is mainly supportive –> fluid and electrolyte management, although dialysis may be required in some cases
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27
Q

risk factors that put a patient at increased risk for developing CIN.

A
  • preexisting disease –> DM, HTN
  • hypovolemic
  • hypoperfusion
  • obesity
  • hepatorenal syndrome
  • hypoxic
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28
Q

CIN Prevalence

A
  • 6% after CT
  • 9% after angiography
  • 4% after IV pyelography
  • LOW incidence in those with normal renal function 0-5%
  • 12-27% in patients with preexisting renal impairment
  • 50% in those with diabetic neuropathy
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29
Q

CIN pathophysiology

A
  • not well understood
  • worsened by hypoxia and hypoperfusion
  • direct toxicity of contrast media which could be related to harmful effects of free radicals and oxidative stress
  • in renal tubules, the 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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30
Q

CIN treatment

A
  • supportive
  • prevention = important
  • benefit vs risk
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31
Q

oliguria in the OR

A
  • sign of inadequate systemic perfusion

- rapid recognition and treatment can help prevent renal insult

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32
Q

monitors used to assess fluid status in OR

A
  • urinary catheter
  • TEE
  • CVP
  • blood pressure
  • SVV (stroke volume variation)
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33
Q

oliguria treatment

A
  • assume pre-renal oliguria is related to fluid until proven otherwise
  • blood
  • diuretics (DO NOT give in the setting of intravascular hypovolemia); furosemide, mannitol
  • selective dopamine DA1 receptor agonists –> causes renal arteriolar vasodilation (fenoldopam or “low dose” dopamine)
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34
Q

CKD in disadvantaged populations

A
  • African, American Indian, Hispanic, Asian, and Aboriginal populations have higher incidences of DM and HTN, leading causes of chronic kidney disease
  • higher risk of developing severe kidney disease and kidney failure
  • Hispanic Americans 1.5 times greater risk
  • ESRD rates 4 fold higher in African Americans compared to US whites
  • Native Americans 1.8 times more likely to be diagnosed with renal failure
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35
Q

eGFR

A
  • estimated glomerular filtration rate
  • calculated using a formula that included a person’s body habitus, age, sex, serum Cr, and race
  • RACIST - now they are finally getting rid of it
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36
Q

SES and cultural factors that increase risk of developing kidney disease.

A
  • language barriers
  • education and literacy levels
  • low income
  • unemployment
  • lack of adequate health insurance
  • certain culture-specific health beliefs and practices
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37
Q

chronic renal failure

A
  • slow, progressive, irreversible
  • decreased functioning nephrons
  • decreased renal blood flow
  • decreased GFR, tubular function, and reabsorptive capacity
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38
Q

common causes of chronic renal failure

A
  • glomerulonephritis (inflammation of glomeruli, autoimmune)
  • pyelonephritis (kidney inflammation)
  • DM
  • vascular or hypertensive insults
  • congenital defects
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39
Q

decreased renal reserve stage

A

asymptomatic until <40% of normal nephrons remain

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40
Q

renal insufficiency stage

A
  • 10-40% of functioning nephrons remain

- compensated, little renal reserve

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41
Q

end-stage renal failure or uremic stage

A
  • > 95% of nephrons are functional
  • GFR is <5-10% of normal
  • severely compromised electrolyte, hematologic, and acid-base balances
  • uremia (urine in blood) is eventually lethal
  • dialysis dependent
42
Q

chronic renal failure clinical manifestations

A
  • hypervolemia
  • acidemia
  • hyperkalemia
  • cardiorespiratory dysfunction
  • anemia
  • bleeding disturbances
43
Q

treatment for chronic renal failure

A
  • hemodialysis
  • peritoneal dialysis
  • kidney transplant
44
Q

glucose

A
  • freely filtered by glomerulus

- reabsorbed in proximal tubule

45
Q

glycosuria

A

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

46
Q

BUN

A
  • blood urea nitrogen
  • not a direct renal function
  • influenced by exercise, bleeding, steroids, and tissue breakdown
  • elevated in kidney disease once GFR is reduced to ~75%
47
Q

serum creatinine

A
  • muscle tissue turnover and dietary intake of protein
  • creatinine is freely filtered at the glomerulus and is neither reabsorbed or secreted
  • best tool to assess kidney function
48
Q

creatinine clearance

A

-good measure of GFR

49
Q

GFR

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

electrocardiogram in renal disease

A
  • reflects toxic effects of potassium excess more closely than determination of serum potassium concentration
  • peaked T waves
  • small or indiscernible P waves
51
Q

hyperkalemia treatment

A
  • CaCl (or gluconate)
  • insulin and D50 (5-10 units and 1 amp)
  • albuterol
  • hyperventilate
52
Q

clinical situations that contribute to increased K+ in renal failure

A
  • protein catabolism
  • hemolysis
  • hemorrhage
  • transfusion of stored RBCs
  • meatbolic acidosis
  • exposure to meds that inhibit K+ entry into cells or K+ secretions in distal nephron
53
Q

stored blood and potassium

A
  • blood storage slow and constant leak of potassium from the cells into plasma due to failure of sodium potassium ATPase pump failure
  • plamsa potassium may increase by 0.5-1 mmol/L per day of refrigerator storage
54
Q

prevention of hyperkalemia following a transfusion

A
  • select blood collected less than 5 days prior to transfusion
  • wash unit of blood immediately before infusion to remove excess potassium
  • use of potassium absorption filters during transfusion
  • rate and volume of transfusion affect potassium level
55
Q

ultrasound + renal disease

A
  • noninvasive
  • minimal patient prep
  • assess kidney size, hydronephrosis, vasculature, obstructions, and masses
56
Q

CT + renal disease

A

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

57
Q

MRI + renal disease

A
  • detailed tissue characterization
  • nice alternative to contrast CT
  • reduced radiation exposure
58
Q

general anesthesia effect on renal function

A

-PPV and decreased CO –> depression of renal blood flow, GFR, urinary flow, and electrolyte secretion

59
Q

regional anesthesia effect on renal function

A

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

60
Q

indirect effects on renal function

A

-circulatory, endocrine, SNS, patient positioning

61
Q

direct effects on renal function

A

medications that target renal cellular function

62
Q

surgery effect on renal function

A

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

63
Q

morphine in renal failure

A
  • active metabolites that depend on renal clearance mechanisms for elimination
  • morphine-3-glucuronide and morphine-6-glucuronide are excreted via kidney
64
Q

meperidine (demerol) in renal failure

A
  • active metabolite normeperidine depends on renal excretion
  • accumulation can lead to CNS toxicity and seizures
65
Q

fentanyl in renal failure

A
  • not grossly altered by renal failure, but decrease in plasma protein binding may result in higher free fractions of drug
  • probably drug of choice in those with renal failure
66
Q

CKD and ketamine

A
  • 8% of administered ketamine metabolized by the liver forming norketamine
  • norketamine hydroxylated into water soluble metabolite and excreted by kidneys
  • most clinicians believe dose modification for ketamine not necessary
67
Q

gapapentenoids in renal failure

A
  • gabapentin, pregabalin
  • liberal administration of gabapentinoids may increase risk of over sedation and even coma
  • these agents do not undergo hepatic metabolism and are excreted SOLEY by the kidney
  • a reduction of 50% of the dose for each 50% decline in GFR or CCr and increasing time interval between doses is advised
68
Q

inhalational agents in renal failure

A
  • all can cause a decrease in blood pressure

- kidneys respond with compensatory increase in renal vascular resistance which decreases renal blood flow

69
Q

isoflurane

A

decreases BP dose dependent

70
Q

desflurane

A

with increased heart rate, may maintain a greater degree of CO and therefore renal perfusion

71
Q

sevoflurane

A
  • free fluoride ion metabolite
  • was more pronounced and only proven with methoxyflurane (and greater than 5 MAC hours)
  • clear evidence not established with sevo
72
Q

compound A

A
  • CO2 absorbents containing soda lime (KOH, NaOH, water, and Ca(OH)2) degrade sevo resulting in production of vinyl ether called compound A
  • routinely used outside US
73
Q

Risk of compound A development dependent on

A
  • duration of gas exposure
  • fresh gas flow rate
  • concentration of sevo
74
Q

amsorb

A
  • replaces soda lime
  • non-caustic and disposed of in domestic waste
  • no compound A production even with low flows of sevo
75
Q

propofol in renal failure

A
  • does not adversely affect renal tubular function
  • may be an extrahepatic site of propofol deposition
  • prolonged infusion may result in green urine due to presence of phenolic metabolites
  • PRIS can result in renal failure secondary to rhabdo, myoglobinuria, hypotension, metabolic acidosis
76
Q

succinylcholine in renal failure

A
  • can be used carefull
  • metabolism catalyzed by pseudocholinesterase to yield the non-toxic end products of succinic acid and choline
  • admin of succ causes rapid, transient increase of 0.5 mEq/L in serum potassium concentration
  • can be exaggerated in those with renal failure
  • ok to use of patient has received dialysis within 24 hours and normal serum K
77
Q

non-depolarizing muscle relaxants in renal failure

A

the duration of action of muscle relaxants may be PROLONGED in patients with renal failure

78
Q

sugammadex in renal failure

A
  • cyclodextrin is the molecule that inactivates aminosteroidal NMBs
  • resultant sugammadex NMB complex is excreted by the kidney
  • in patients with severe renal disease, these complexes can accumulate
  • insufficient data on what long term exposure to the complexes means
79
Q

sodium nitroprusside in renal failure

A
  • thiocyanate is final metabolic product
  • half life normally more than 4 days, but can be prolonged in renal failure
  • thiocyanate levels greater than 10 mg/dL = toxic
  • hypoxia, nausea, tinnitus, muscle spasm, disorientation, psychosis
80
Q

albumin in renal failure

A

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

81
Q

hetastarch/dextran in renal failure

A

NOT FRIEND
-have been associated with acute kidney injury secondary to breakdown of synthetic carbs to degradation products that cause direct tubular injury and plugging of tubules

82
Q

dopaminergics

A
  • dopamine and fenoldopam

- dilate afferent and efferent arterioles and increase renal perfusion

83
Q

anti-dopaminergics

A
  • metoclopramide, phenothiazines, doperiodol

- may impair renal response to dopamine

84
Q

renal cell carcinoma

A
  • most common renal malignancy (80% of all solid renal masses)
  • originates in lining of proximal tubules
  • refractory to chemo or radiation
  • surgical treatment is curative (often only option)
  • 5-10% of patients, tumor extends into renal vein and IVC + RA –> may require CPB
85
Q

classic triad presentation of renal cell carcinoma

A
  • hematuria
  • flank pain
  • renal mass
86
Q

renal dysplasia

A
  • malformation in tubules during fetal development
  • 1 in 4000 live births
  • kidney has irregular cysts of varying sizes
  • diagnosis by ultrasound in utero
  • may also have ureteropelvic junction obstruction and vesicoureteral reflux
  • linked to genetic mutation and illicit drug use by mother (cocain)
  • bilateral = incompatible with life
  • 90% of patients will have contralateral hypertrophy by adulthood
  • leads to CKD, dialysis, and transplant
87
Q

polycystic kidney disease (PKD)

A
  • inherited (dominant or recessive), massive enlargement of the kidneys with compromised renal function
  • cysts can also occur on other organs
  • painful due to distention of cysts and stretching of fascia
  • hemorrhage, rupture or infection exacerbate the pain
88
Q

complications of PKD

A
  • hypertension due to activation of RAAS
  • cyst infections
  • bleeding
  • decline in renal function
89
Q

treatment PKD

A
  • symptom management
  • dialysis
  • transplant
90
Q

wilms tumor (nephroblastoma)

A
  • often presents unilaterally and a painless palable abdominal mass (<5% bilateral)
  • can be associated with congenital or genetic defects
  • most common malignant renal tumor in kids
  • requires resection of possible chemo
  • capacity for rapid growth
  • metastasis usually to lungs
91
Q

stage 1 wilms tumor

A

43% of cases

limited to kidney and is completely excised

92
Q

stage 2 wilms tumor

A

23% of cases

tumor extends beyond kidney but completely excised

93
Q

stage 3 wilms tumor

A

20% of cases

inoperable primary tumor or lymph node metastasis

94
Q

stage 4 wilms tumor

A

lymph node metastases outside abdomino-pelvic region

95
Q

stage 5 wilms tumor

A

bilateral renal involvement

96
Q

total nephrectomy

A
  • renal artery and vein ligated and then it involves removal of kidney, ipsilateral adrenal gland, perinephric fat, and surrounding fascia
  • other kidney must be functional
97
Q

partial nephrectomy

A
  • nephron sparing
  • considered for patients with a solitary functional kidney , small lesions (<4 cm), or bilateral tumors, OR patients with increased risk because of disease (DM, HTN)
  • maybe open, laparoscopic, or robotic
98
Q

pre-surgery

A
  • flank mass
  • HTN - started on antihypertensives
  • ultrasound and CT
  • biopsy -diagnosis
99
Q

anesthesia for renal

A
  • premed
  • BP control –> wide fluctuations requiring volume and vasopressors
  • PIVsx2, aline, CVC palced by surgeon if chemo or by anesthesia for IV immunosuppression med
100
Q

anesthetic considerations for nephrectomy

A
  • standard risk assessment
  • ID smoking and age risk factors
  • note any preexisting renal dysfunction
  • many are anemic - CBC and T+C
  • K+ = BMP
  • regional anesthesia include blockage of nerve roots T8-L3
  • ERAS
  • opioid sparing

N935 Advanced Pathophysiology II (16 decks)

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