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Basics of Anesthesia > Week 10 - Renal Physiology and Anesthesia > Flashcards

Week 10 - Renal Physiology and Anesthesia Flashcards

1
Q

What are the different homeostatic processes the renal system plays a vital role in?

A 
– Regulation of H2O and electrolyte balance
– Regulation of body fluid osmolality
– Electrolyte composition in the body
– Excretion of metabolic wastes
– Regulation of arterial blood pressure
– Secretion of hormones
– Bone metabolism
– Hematopoiesis (erythropoietin)
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2
Q

What are the two major layers of the kidney?

A

Outer Cortex and Inner Medulla

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3
Q

What is the nephron of the kidney?

A

Functional unit of the kidney

  • each kidney contains 1 million nephrons
  • body cant regenerate nephrons
  • after age 40 the number of nephrons decreases by 10% for every 10 years of age
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4
Q

What are the 6 major components of a nephron?

A 
– Glomerulus
– Proximal convoluted tubule
– Loop of Henle
– Distal renal tubule
– Collecting tubule
– Juxtaglomerular apparatus
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5
Q

What are the characteristics of the glomerulus?

A 
– Network of capillaries
– High hydrostatic pressure of 60 mmHg
– Covered with epithelial cells
– Encased in bowman's capsule (Filtered fluid enters Bowman's capsule 
and then the proximal tubule)
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6
Q

What are the characteristics of the long tubule of the kideny?

A 
– Proximal tubule lies in the 
renal cortex
– Loop dips into the renal 
medulla and forms the loop 
of henle --- Thin walled
– The ascending loop goes 
back into the cortex --- Thick walled
– Terminates in short segment called the macula densa
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7
Q

What are the two classes of nephrons?

A 
Cortical Nephron (80%): short nephron loop and glomerulus further from the corticomedullary junction
-efferent arteriole supplies peritubular capillaries
Juxtamedullary Nephron (20%): has long nephron loop and glomerulus closer to the corticomedullary junction
-efferent arteriole supplies vasa recta
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8
Q

What are the different mechanisms of renal excretion?

A

Glomerular Filtration: large amounts of protein free fluid are filtered into Bowman’s Capsule

Reabsorption: filtered substances are reabsorbed from the tubules and back into the blood

Secretion: some substances are secreted into the renal tubule so that the amount in the urine is greater than the amount found in the glomerular filtrate

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9
Q

What is glomerular filtration determined by?

A

Hydrostatic and Colloid Osmotic forces across the glomerular capillary basement membrane

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10
Q

What is the function of the glomerular capillary basement membrane?

A
  • Restricts filtration of substances with a large molecular size
  • It is negatively charged thus prevents the filtration of negatively charged substances
  • some plasma proteins like albumin are negatively charged and the charge not the size prevents filtration
  • early in some renal diseases, this negative charge is lost and proteinuria occurs
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11
Q

What are determinants of GFR?

A
  • Hydrostatic pressure in the glomerular capillaries
  • Hydrostatic pressure in Bowman’s capsule
  • Glomerular capillary colloid osmotic pressure
  • Bowman’s capsule colloid osmotic pressure — GFR = Pcap - (PBC + COPcap)
  • Normal is 120mL/min
  • life threatening when GFR is < 30 mL/min
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12
Q

What does the measurement of GFR tell you?

A

Renal Clearance – way of quantifying how efficiently the kidney clears the blood of various substances

  • can use inulin (polymer of fructose that is not produced in the body and isn’t metabolized)
  • Creatinine is a convenient way because no artificial substance is necessary
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13
Q

What percent of cardiac output supplies the kidneys?

A

20-25% of cardiac output (normal is 1200mL/min)

  • renal artery comes off aorta and enters the hilum – branches to form the interlobar arteries, arcuate arteries, interlobular arteries and arterioles
  • 90% renal blood flood is to the cortex and 10% is to the medulla
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14
Q

What determines renal blood flow?

A

The pressure gradient across the renal vasculature

RBF = (renal artery pressure - renal vein pressure) / total renal vascular resistance

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15
Q

What two mechanisms control autoregulation of the renal system?

A

Tubuloglomerular Feedback

Myogenic mechanism achieves autoregulation by changing renal vascular resistance as the arterial blood pressure changes

*urine output is NOT autoregulated

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16
Q

What pressure range is renal blood flow and GFR autoregulated between?

A

80 - 180 mmHg

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17
Q

What are the regulators of renal blood flow increase RBF or GFR?

A
  • Prostaglandins: appear protective and prevent renal vasoconstriction/ischemia
  • Nitric oxide: increases RBF and GFR
  • Bradykinin: locally produced vasodilator (increases RBF and GFR)
  • Atrial Natriuretic Peptide: secreted by heart with HTN and expanded blood volume (increases GFR)
  • Dopamine: proximal tubule produces dopamine (increases RBF and inhibits renin release)
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18
Q

What are the regulators of renal blood flow decrease RBF or GFR?

A
  • Sympathetic nerves: SNS stimulation = vasoconstriction in both afferent and efferent arterioles (decreases RBF and GFR)
  • Angiotensin II: constricts afferent and efferent arterioles
  • Endothelin: potent vasoconstrictor of both afferent and efferent arterioles (may be responsible for some renal damage in DMII)
  • Adenosine: decreases RBF and GFR by causing vasoconstriction of the afferent arteriole
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19
Q

What are the three principles of membrane transport?

A

Passive Transport – doesn’t require energy, moves down concentration gradient

Facilitated Diffusion – involves a membrane transporter, moves with and against electrochemical gradients

Active Transport – requires energy in the form of ATP, sodium/potassium pump most common active transport in the kidney

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20
Q

What is a transport maximum?

A

Most substances that are actively secreted or reabsorbed have a limit on the rate of transport (occurs due to saturation of transport system)

  • Glucose: transport max is approx 250-300mg/dL (glucosuria occurs when level exceeds this)
  • Creatinine also has transport max
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21
Q

What are the functions of the proximal tubule?

A
  • Sodium Reabsorption (Major function) – 67% of solute reabsorption, facilitated transport transport from tubule to cell
  • Reabsorption of glucose, potassium, calcium, phosphate, uric acid and urea
  • Water reabsorption – driving pressure is the osmotic gradient created as solute is reabsorbed
  • Protein reabsorption – normally filtered and reabsorbed, easily saturated and found in urine if significant amount present (early sign of renal disease)
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22
Q

What can occur if a patient is taking two organic anions or two organic cations?

A

Excretion may be delayed

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23
Q

What is the function of the loop of Henle?

A
  • Water reabsorbed in descending loop
  • Thick ascending loop is impermeable to water but solute reabsorption occurs
  • Loop diuretics work by inhibiting the reabsorption of Na in the ascending loop (reabsorption of K and Mg is also inhibited)
  • Because solute and not water is reabsorbed in ascending loop the osmolality of tubular fluid is reduced
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24
Q

What is the juxtaglomerular complex?

A

Formed by the first part of the distal tubule

Provides feedback control of GFR and RBF

Divided into cortical and medullary portions

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25
Q

What is the function of the cortical tubules?

A

– Secrete K+
– Aldosterone mediated Na+ reabsorption
– Acid-base balance
– Freely permeable to urea

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26
Q

What is the function of the medullary tubules?

A

Normally impermeable to water but in the presence of ADH, water is reabsorbed

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27
Q

What are four factors that affect the kidneys ability to concentrate urine?

A
  • Countercurrent mechanism
  • Impermeability of thick ascending loop of Henle to water
  • ADH: increases water reabsorption in the distal nephron
  • Active reabsorption of NaCl in the ascending loop of Henle
28
Q

What is the countercurrent multiplier in the renal system?

A
  • Renders the renal medullary interstitium hypertonic — normal body osmolarity is 275-295 mOsm/L (renal interstitium is 1200)
  • Loop of Henle has 2 parallel limbs – “Countercurrent”
  • Fluid into medulla: IN: descending limb OUT: ascending limb
  • Vasa recta reabsorbs water and transports solute
  • Accumulation of NaCl in the interstitium is critical and a standing osmotic gradient is established
29
Q

What is the lower limit of urine output in order to excrete necessary wastes?

A

500 mL/day (with maximum water reabsorption)

30
Q

What SNS level is the renal cortex and vasculature innervated by?

A

SNS Fibers T4-L1

  • mild alpha adrenergic stimulation = efferent arteriolar constriction (preserves GFR)
  • intense alpha adrenergic stimulation = afferent arteriolar vasoconstriction (decreases GFR)
31
Q

Where is renin produced? When is it released?

A

Produced in cells of JG apparatus

Released due to several stimuli:

  • decreased renal artery perfusion pressure
  • SNS stimulation
  • decreased NaCl in macula densa

*Renin alone has no physiologic function (acts as proteolytic enzyme – cleaves angioteninogen to form angiontensin I which is cleaved to angiotensin II by ACE)

32
Q

What are the effects of Angiotensin II?

A

Overall effect is increase water and Na reabsorption and return circulating volume to normal

Other effects:

  • stimulation of aldosterone release by adrenal cortex
  • arterial vasoconstriction which increases BP
  • stimulation of ADH secretion and thirst
  • enhances reabsorption of NaCl in prox tubule
  • in severe stress (shock)- large amts of Angio II cause intense renal artery constriction and decreased RBF
  • increases intrarenal prostaglandins

*ACE Inhibitors reduce renal vascular resistance

33
Q

What is aldosterone secreted from? What is its function?

A

Secreted by Zona Glomerulosa of adrenal cortex in response to hyperkalemia, Angio II, and ACTH

Acts on ascending loop of Henle, distal tubule and collecting ducts – increases reabsorption of Na and Cl (causes water to passively follow)

Overall effects is increase Na and water reabsorption from distal tubule

34
Q

Where is antidiuretic hormone synthesized? Where does it act? What does it cause?

A

Synthesized by anterior hypothalamus

When released it acts of receptors in collecting ducts – increases water reabsorption leading to more concentrated urine

Causes increased NaCl reabsorption in ascending loop of Henle – increases medullary osmolarity and further promotes water reabsorption

35
Q

What effect does atrial natriuretic peptide have on the renal system?

A
  • Released from the atrium in response to local wall stretch and increased atrial volume
  • Increases GFR and promotes water and Na excretion
  • Inhibits release of renin (blocks effect of renin on angio I and the vasoconstriction produced by angio II)

*overall effects of ANP are opposite and opposed to renin, angiotensin, ADH and aldosterone

36
Q

Where are Dopamine-1 receptors located? What is the effect when low dose Dopamine is infused (1-3mcg/kg/min)?

A

Located in renal vasculature and proximal renal tubule

Low Dose (1-3 mcg/kg/min) = increased RBF and GFR and increased Na excretion and diuresis
*>10 mcg/kg/min = renal vasoconstriction and decreased GFR
37
Q

What spinal level innervates the ureters and kidneys?

A

Primarily T8-L2

*nerve supply to pelvic organs (bladder, prostate, seminal vesicles, and urethra) is primarily lumbosacral with some thoracic innervation

38
Q

What are indications for a cystoscopy?

A

Hematuria
Recurrent UTIs
Renal calculi
Urinary obstruction

*most common urological procedure

39
Q

What are intraop considerations for cystoscopy?

A

Lithotomy Position!

  • failure to properly position pt can result in iatrogenic injuries
  • leg position maintained using straps around ankles or special holders to support legs

*positioning is everyones responsibility

40
Q

What is the most common nerve injury associated with the lithotomy position?

A

Brachial Plexus

41
Q

What physiological changes are seen with cystoscopy?

A
  • Decreased FRC (atelectasis and hypoxis, accentuated by trendelenburg >30*)
  • Exacerbation of CHF (elevation of legs increases venous return acutely, MAP increases, but CO doesn’t change significantly)
  • Hypotension (rapid lowering of legs acutely decreases venous return, vasodilation from either general or regional anesthesia may worsen it)
42
Q

What are considerations of regional anesthetic management for cystoscopy?

A

Spinal vs Epidural – spinal most preferred (faster onset, shorter duration)
*adequate sensory blockade may take 15-20 min for Epidural vs 5 min for spinal

Sensory level to T10 necessary

Obturator reflex (external rotation and adduction of the thigh) - only reliably blocked by muscle paralysis during GA

43
Q

What are the indications for a Trans Urethral Resection of Prostate (TURP)?

A
  • Benign Prostatic Hypertrophy (BPH) - symptomatic bladder outlet obstruction (usually men >60yr)
  • Severe urinary tract symptoms refractory to medical therapy
  • Persistent gross hematuria
  • Recurrent UTIs
  • Renal insufficiency
  • Bladder stones
44
Q

What are complications of TURP procedures?

A
  • Hemorrhage (more common w/ glands >40mL in size, difficult to control bleeding through cystoscope)
  • Bladder Perforation
  • Septicemia
  • Hypothermia
  • DIC
  • MI
  • Pulmonary edema
  • Renal failure
  • TURP syndrome
45
Q

What is the pathogenesis behind TURP syndrome?

A

Open venous sinuses in the prostate allow for potential systemic absorption of the irrigating fluid – hypotonic (mostly H2O) irrigation

Absorption of >2L = TURP Syndrome

46
Q

What are the symptoms of TURP Syndrome?

  • CV and Respiratory
  • CNS
  • Metabolic
  • Other
A

CV and Respiratory: HTN, brady/tachyarrhythmia, CHF, pulmonary edema, hypoxemia, hypotension

CNS: agitation/confusion, seizures, coma, visual disturbance/blindness

Metabolic: hyponatremia, hyperglycemia, hyperammonemia

Other: hypoosmolality, hemolysis, intravascular volume expansion

47
Q

How do you treat TURP Syndrome?

A
  • Early recognition is vital
  • Absorbed H2O must be eliminated (fluid restriction, loop diuretic)
  • Avoid hypoxemia and hypoperfusion
  • Treat symptomatic hyponatremia (hypertonic saline, amount based on serum Na level)
  • Treat seizure activity (small doses of versed, diazepam, or thiopental)
  • Intubation (advisable to prevent aspiration until mental status returns to normal
48
Q

What are intraop considerations for TURP procedures?

A
  • Hypothermia – large amounts of irrigating fluid at room temp = heat loss
  • Bladder Perforation – signaled by poor return of irrigating fluid, sudden HoTN, bradycardia
  • Coagulopathy (DIC) – result from release of thromboplastins
  • Septicemia – prophylactic antibiotic therapy prior to TURP
49
Q

What are benefits of spinal or epidural anesthetic management for TURP procedures?

A
  • Provides excellent anesthesia and good operating conditions
  • Allows for more immediate detection of signs of TURP syndrome and bladder perforation
  • Acute hyponatremia from TURP syndrome may delay or prevent emergence from GA
  • contraindicated with metastasis to lumbar spine
  • need T10 level
50
Q

What are postop considerations for TURP procedures?

A
  • If TURP syndrome: obtain serum osmolarity, CXR, EKG, electrolytes
  • Fever/bacteremia/sepsis
  • Prevent Hypothermia -Shivering (dislodges clots, promotes bleeding)
  • Hemodilution from absorption of irrigation (transient decrease in hematocrit)
  • Foot drop: peroneal nerve compression at lateral fibular head while in lithotomy position
51
Q

What is extracorporeal shock wave lithotripsy (ESWL) a treatment for?

A

Treatment of kidney stones and stones in upper 2/3 of the ureters
-used more for larger stones (>4mm) that are intrarenal

Repetitive high energy shock waves focus on stone – stone is fragmented and usually passed through urinary tract

52
Q

What are preop considerations for extracorporeal shock wave lithotripsy (ESWL)?

A

-Pt with cardiac arrhythmia hx or with pacemaker/ICD are at increased risk for arrhythmias induced by ESWL

Shock waves can damage components of pacemaker/ICD

Synchronization of the shock waves to the R wave from the ECG decreases the incidence of arrhythmias

53
Q

What are disadvantages of using regional anesthesia for extracorporeal shock wave lithotripsy (ESWL) procedures?

A

Need T6 level to ensure adequate anesthesia

Inability to control diaphragmatic movement (may prolong the procedure) – GA allows for control of breathing

Bradycardia from high sympathetic blockade also prolongs the procedure – shock waves are coupled to ECG

54
Q

What are contraindications to extracorporeal shock wave lithotripsy (ESWL) procedures?

A
  • Inability to position patient so lung and intestine are away from the shock wave
  • Urinary obstruction below the stone
  • Untreated infection
  • Bleeding diathesis
  • Pregnancy
  • Aortic aneurysm +/-
55
Q

What drugs should you avoid in renal transplant surgery?

A 
Succinylcholine if K >5
Morphine due to metabolite
Meperidine due to metabolite
NSAIDs
COX-2 inhibitors
Enflurane

*use rocuronium, vec, mivacurium, and pancuronium with caution

56
Q

What is Serum Creatinine level a useful marker of?

A

Useful marker of GFR
-if creatinine doubles, GFR has decline by 50%

  • product of skeletal muscle catabolism
  • Normal = 0.8-1.2
  • Creatinine Clearance normal = 120 mL/min
57
Q

BUN level is useful in assessing what?

A

Prerenal vs Intrarenal abnormalities

  • urea = most abundant metabolic waste product
  • BUN increases when GFR is reduced
  • Normal = 8-10
58
Q

What is the minimum allowable urine output for adequate excretion of metabolic wastes?

A

0.5 mL/kg/hr

59
Q

What are the three types of acute renal failure?

A

Prerenal - Disorder of systemic circulation that cause hypoperfusion

Infrarenal - Destruction of lining of renal tubules d/t nephrotoxins or renal ischemia (most common cause in critically ill patients)

Postrenal - Obstruction may occur anywhere from renal pelvis to distal urethra – Less than 5 % of cases

60
Q

What are the different stages of chronic kidney disease?

A

Stage 1 – Kidney damage, but normal GFR (>90ml/min)
Stage 2 – Mild Kidney damage (GFR 60-89 ml/min
Stage 3- Moderate kidney damage (GFR 30-59 ml/min)
Stage 4- Severe kidney damage (GFR 15-29 ml/min)
Stage 5- Kidney failure (GFR <15 ml/min or ESRD – On renal replacement therapy)

61
Q

What causes anemia of chronic renal failure? Which way does the oxyhgb dissociation curve shift?

A

Decreased erythropoietin and hemolysis

Shift oxyhgb dissociation curve to RIGHT due to increased 2-3 DPG

62
Q

What coagulopathies are seen in chronic renal failure?

A

Decreased platelet adhesiveness due to metabolic acidosis interfering with Factor VIII

*treat with desmopressin or cryoprecipitate

63
Q

What electrolyte disturbances are seen in chronic renal failure?

A
  • Hyperkalemia
  • Hypermagnesemia
  • Hypocalcemia (decreased Ca absorption due to inability to activate vitamin D)
64
Q

How does renal disease affect Propofol, Etomidate, Benzos, and Opioids?

A

Propofol: pharmacokinetics not altered, no drug accumulation, no unusual hemodynamic effects

Etomidate: decreased protein binding w/ hypoalbuminemia may enhance its effects

Benzos: highly protein bound and increased sensitivity w/ hypoalbuminemia

Opioids: inactivated in liver -p accumulation of active metabolites

65
Q

What are manifestations of uremia?

A
  • Confusion
  • Lethargy
  • Seizures
  • Volume overload / CHF
  • HTN
  • Arrhythmia
  • Hyperventilation / Dyspnea
  • Metabolic Acidosis
  • Hyperkalemia/ Hyponatremia/ Hypermagnesemia
  • Anemia / Platelet dysfunction
66
Q

What are indications for dialysis?

A
  • Fluid overload
  • Hyperkalemia
  • Severe acidosis
  • Metabolic encephalopathy
  • Pericarditis
  • Coagulopathy
  • Drug toxicity

Basics of Anesthesia (35 decks)

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